PMID- 30971393
OWN - NLM
STAT- MEDLINE
DCOM- 20190418
LR  - 20190418
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Linking)
VI  - 365
DP  - 2019 Apr 10
TI  - Incidence of type 2 diabetes mellitus in men receiving steroid 5alpha-reductase
      inhibitors: population based cohort study.
PG  - l1204
LID - 10.1136/bmj.l1204 [doi]
AB  - OBJECTIVE: To investigate the incidence of new onset type 2 diabetes mellitus in 
      men receiving steroid 5alpha-reductase inhibitors (dutasteride or finasteride)
      for long term treatment of benign prostatic hyperplasia. DESIGN: Population based
      cohort study. SETTING: UK Clinical Practice Research Datalink (CPRD; 2003-14) and
      Taiwanese National Health Insurance Research Database (NHIRD; 2002-12).
      PARTICIPANTS: Men in the CPRD who received dutasteride (n=8231), finasteride
      (n=30 774), or tamsulosin (n=16 270) were evaluated. Propensity score matching
      (2:1; dutasteride to finasteride or tamsulosin) produced cohorts of 2090, 3445,
      and 4018, respectively. In the NHIRD, initial numbers were 1251 (dutasteride),
      4194 (finasteride), and 86 263 (tamsulosin), reducing to 1251, 2445, and 2502,
      respectively, after propensity score matching. MAIN OUTCOMES MEASURE: Incident
      type 2 diabetes using a Cox proportional hazard model. RESULTS: In the CPRD, 2081
      new onset type 2 diabetes events (368 dutasteride, 1207 finasteride, and 506
      tamsulosin) were recorded during a mean follow-up time of 5.2 years (SD 3.1
      years). The event rate per 10 000 person years was 76.2 (95% confidence interval 
      68.4 to 84.0) for dutasteride, 76.6 (72.3 to 80.9) for finasteride, and 60.3
      (55.1 to 65.5) for tamsulosin. There was a modest increased risk of type 2
      diabetes for dutasteride (adjusted hazard ratio 1.32, 95% confidence interval
      1.08 to 1.61) and finasteride (1.26, 1.10 to 1.45) compared with tamsulosin.
      Results for the NHIRD were consistent with the findings for the CPRD (adjusted
      hazard ratio 1.34, 95% confidence interval 1.17 to 1.54 for dutasteride, and
      1.49, 1.38 to 1.61 for finasteride compared with tamsulosin). Propensity score
      matched analyses showed similar results. CONCLUSIONS: The risk of developing new 
      onset type 2 diabetes appears to be higher in men with benign prostatic
      hyperplasia exposed to 5alpha-reductase inhibitors than in men receiving
      tamsulosin, but did not differ between men receiving dutasteride and those
      receiving finasteride. Additional monitoring might be required for men starting
      these drugs, particularly in those with other risk factors for type 2 diabetes.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not
      already granted under a licence) please go to
      http://group.bmj.com/group/rights-licensing/permissions.
FAU - Wei, Li
AU  - Wei L
AD  - Research Department of Practice and Policy, School of Pharmacy, University
      College London, London, UK.
FAU - Lai, Edward Chia-Cheng
AU  - Lai EC
AD  - School of Pharmacy, Institute of Clinical Pharmacy and Pharmaceutical Sciences,
      College of Medicine, National Cheng Kung University, Tainan City, Taiwan.
FAU - Kao-Yang, Yea-Huei
AU  - Kao-Yang YH
AD  - School of Pharmacy, Institute of Clinical Pharmacy and Pharmaceutical Sciences,
      College of Medicine, National Cheng Kung University, Tainan City, Taiwan.
FAU - Walker, Brian R
AU  - Walker BR
AD  - University/BHF Centre for Cardiovascular Science, Queen's Medical Research
      Institute, University of Edinburgh, Edinburgh EH16 4TJ, UK.
AD  - Institute of Genetic Medicine, International Centre for Life, Newcastle
      University, Newcastle upon Tyne, UK.
FAU - MacDonald, Thomas M
AU  - MacDonald TM
AD  - Medicines Monitoring Unit, Ninewells Hospital and Medical School, Dundee, UK.
FAU - Andrew, Ruth
AU  - Andrew R
AUID- ORCID: http://orcid.org/0000-0002-6916-2994
AD  - University/BHF Centre for Cardiovascular Science, Queen's Medical Research
      Institute, University of Edinburgh, Edinburgh EH16 4TJ, UK ruth.andrew@ed.ac.uk.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20190410
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
RN  - 0 (5-alpha Reductase Inhibitors)
RN  - 57GNO57U7G (Finasteride)
RN  - G3P28OML5I (Tamsulosin)
RN  - O0J6XJN02I (Dutasteride)
SB  - AIM
SB  - IM
MH  - 5-alpha Reductase Inhibitors/*adverse effects/therapeutic use
MH  - Aged
MH  - Aged, 80 and over
MH  - Diabetes Mellitus, Type 2/*chemically induced/*epidemiology
MH  - Dutasteride/adverse effects/therapeutic use
MH  - Finasteride/adverse effects/therapeutic use
MH  - Humans
MH  - Incidence
MH  - Male
MH  - Middle Aged
MH  - Prostatic Hyperplasia/complications/*drug therapy
MH  - Tamsulosin/adverse effects/therapeutic use
COIS- Competing interests: All authors have completed the ICMJE uniform disclosure form
      at www.icmje.org/coi_disclosure.pdf and declare: no support from any organisation
      for the submitted work; no financial relationships with any organisations that
      might have an interest in the submitted work in the previous three years; no
      other relationships or activities that could appear to have influenced the
      submitted work.
EDAT- 2019/04/12 06:00
MHDA- 2019/04/19 06:00
CRDT- 2019/04/12 06:00
PHST- 2019/04/12 06:00 [entrez]
PHST- 2019/04/12 06:00 [pubmed]
PHST- 2019/04/19 06:00 [medline]
AID - 10.1136/bmj.l1204 [doi]
PST - epublish
SO  - BMJ. 2019 Apr 10;365:l1204. doi: 10.1136/bmj.l1204.

PMID- 30967375
OWN - NLM
STAT- MEDLINE
DCOM- 20190418
LR  - 20190418
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Linking)
VI  - 365
DP  - 2019 Apr 9
TI  - Efficacy and safety of dual SGLT 1/2 inhibitor sotagliflozin in type 1 diabetes: 
      meta-analysis of randomised controlled trials.
PG  - l1328
LID - 10.1136/bmj.l1328 [doi]
AB  - OBJECTIVE: To assess the efficacy and safety of dual sodium glucose cotransporter
      (SGLT) 1/2 inhibitor sotagliflozin in type 1 diabetes mellitus. DESIGN:
      Meta-analysis of randomised controlled trials. DATA SOURCES: Medline; Cochrane
      Library; Embase; international meeting abstracts; international and national
      clinical trial registries; and websites of US, European, and Japanese regulatory 
      authorities, up to 10 January 2019. ELIGIBILITY CRITERIA FOR SELECTING STUDIES:
      Randomised controlled trials evaluating the effect of sotagliflozin versus active
      comparators or placebo on glycaemic and non-glycaemic outcomes and on adverse
      events in type 1 diabetes in participants older than 18. Three reviewers
      extracted data for study characteristics, outcomes of interest, and risk of bias 
      and summarised strength of evidence using the grading of recommendations
      assessment, development, and evaluation approach. Main outcomes were pooled using
      random effects models. RESULTS: Of 739 records identified, six randomised placebo
      controlled trials (n=3238, duration 4-52 weeks) were included. Sotagliflozin
      reduced levels of glycated haemoglobin (HbA1c; weighted mean difference -0.34%
      (95% confidence interval -0.41% to -0.27%), P<0.001); fasting plasma glucose
      (-16.98 mg/dL, -22.1 to -11.9; 1 mg/dL=0.0555 mmol/L) and two hour-postprandial
      plasma glucose (-39.2 mg/dL, -50.4 to -28.1); and daily total, basal, and bolus
      insulin dose (-8.99%, -10.93% to -7.05%; -8.03%, -10.14% to -5.93%; -9.14%,
      -12.17% to -6.12%; respectively). Sotagliflozin improved time in range (weighted 
      mean difference 9.73%, 6.66% to 12.81%) and other continuous glucose monitoring
      parameters, and reduced body weight (-3.54%, -3.98% to -3.09%), systolic blood
      pressure (-3.85 mm Hg, -4.76 to -2.93), and albuminuria (albumin:creatinine ratio
      -14.57 mg/g, -26.87 to -2.28). Sotagliflozin reduced hypoglycaemia (weighted mean
      difference -9.09 events per patient year, -13.82 to -4.36) and severe
      hypoglycaemia (relative risk 0.69, 0.49 to 0.98). However, the drug increased the
      risk of ketoacidosis (relative risk 3.93, 1.94 to 7.96), genital tract infections
      (3.12, 2.14 to 4.54), diarrhoea (1.50, 1.08 to 2.10), and volume depletion events
      (2.19, 1.10 to 4.36). Initial HbA1c and basal insulin dose adjustment were
      associated with the risk of diabetic ketoacidosis. A sotagliflozin dose of 400
      mg/day was associated with a greater improvement in most glycaemic and
      non-glycaemic outcomes than the 200 mg/day dose, without increasing the risk of
      adverse events. The quality of evidence was high to moderate for most outcomes,
      but low for major adverse cardiovascular events and all cause death. The
      relatively short duration of trials prevented assessment of long term outcomes.
      CONCLUSIONS: In type 1 diabetes, sotagliflozin improves glycaemic and
      non-glycaemic outcomes and reduces hypoglycaemia rate and severe hypoglycaemia.
      The risk of diabetic ketoacidosis could be minimised by appropriate patient
      selection and down-titration of the basal insulin dose.
CI  - Published by the BMJ Publishing Group Limited. For permission to use (where not
      already granted under a licence) please go to
      http://group.bmj.com/group/rights-licensing/permissions.
FAU - Musso, Giovanni
AU  - Musso G
AUID- ORCID: http://orcid.org/0000-0002-8569-2872
AD  - Humanitas University Gradenigo Hospital, 8 Corso Regina Margherita, 10132 Turin, 
      Italy giovanni_musso@yahoo.it.
FAU - Gambino, Roberto
AU  - Gambino R
AD  - Laboratory of Diabetes and Metabolic Disorders, Department of Medical Sciences,
      University of Turin, Turin, Italy.
FAU - Cassader, Maurizio
AU  - Cassader M
AD  - Laboratory of Diabetes and Metabolic Disorders, Department of Medical Sciences,
      University of Turin, Turin, Italy.
FAU - Paschetta, Elena
AU  - Paschetta E
AD  - Humanitas University Gradenigo Hospital, 8 Corso Regina Margherita, 10132 Turin, 
      Italy.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Meta-Analysis
DEP - 20190409
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
RN  - 0 (Blood Glucose)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (Glycosides)
RN  - 0 (Sodium-Glucose Transporter 2 Inhibitors)
RN  - 6B4ZBS263Y
      ((2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-ethoxybenzyl)phenyl)-6-(methylthio)tetrahydro-
      2H-pyran-3,4,5-triol)
SB  - AIM
SB  - IM
MH  - Blood Glucose/analysis
MH  - Blood Glucose Self-Monitoring/methods
MH  - Diabetes Mellitus, Type 1/*drug therapy/epidemiology
MH  - Diabetic Ketoacidosis/chemically induced/epidemiology
MH  - Dose-Response Relationship, Drug
MH  - Glycated Hemoglobin A/drug effects
MH  - Glycosides/administration & dosage/adverse effects/*therapeutic use
MH  - Humans
MH  - Hypoglycemia/*prevention & control
MH  - Outcome Assessment (Health Care)
MH  - Randomized Controlled Trials as Topic
MH  - Risk
MH  - Sodium-Glucose Transporter 2 Inhibitors/administration & dosage/adverse
      effects/*therapeutic use
COIS- Competing interests: All authors have completed the ICMJE uniform disclosure form
      at www.icmje.org/coi_disclosure.pdf and declare: no support from any organisation
      for the submitted work; no financial relationships with any organisations that
      might have an interest in the submitted work in the previous three years; no
      other relationships or activities that could appear to have influenced the
      submitted work.
EDAT- 2019/04/11 06:00
MHDA- 2019/04/19 06:00
CRDT- 2019/04/11 06:00
PHST- 2019/04/11 06:00 [entrez]
PHST- 2019/04/11 06:00 [pubmed]
PHST- 2019/04/19 06:00 [medline]
AID - 10.1136/bmj.l1328 [doi]
PST - epublish
SO  - BMJ. 2019 Apr 9;365:l1328. doi: 10.1136/bmj.l1328.

PMID- 30972800
OWN - NLM
STAT- Publisher
LR  - 20190411
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
DP  - 2019 Apr 10
TI  - Lipid profile is associated with treatment regimen in a large cohort of children 
      and adolescents with Type 1 diabetes mellitus: a study from the international
      SWEET database.
LID - 10.1111/dme.13963 [doi]
AB  - AIMS: To examine the effect of pump vs injection therapy on the lipid profile of 
      children with Type 1 diabetes mellitus. METHODS: A cross-sectional analysis of
      the lipid profile of children aged </= 18 years with Type 1 diabetes mellitus
      from SWEET, an international diabetes registry, was conducted with a focus on the
      effect of treatment regimen. Dyslipidaemia was defined as LDL cholesterol >/=2.6 
      mmol/l or non-HDL cholesterol >/=3.1 mmol/l. LDL and non-HDL cholesterol values
      among 14 290 children (52% boys, 51% receiving pump therapy) from 60 SWEET
      centres were analysed by linear and logistic regression analysis adjusted for
      sex, age, diabetes duration, HbA1c and BMI-standard deviation score group,
      region, and common interactions between age, sex, HbA1c and BMI. RESULTS: This
      study confirmed the established associations of increased lipids with female sex,
      age, diabetes duration, HbA1c and BMI. LDL and non-HDL cholesterol levels were
      lower in the pump therapy group compared to the injection therapy group [LDL
      cholesterol: injection therapy 2.44 mmol/l (95% CI 2.42 to 2.46) vs pump therapy 
      2.39 mmol/l (95% CI 2.37-2.41), P<0.001; non-HDL cholesterol: injection therapy
      2.88 mmol/l (95% CI 2.86 to 2.90) vs pump therapy 2.80 mmol/l (95% CI 2.78-2.82),
      both P<0.0001]. Similarly, the odds ratios for LDL cholesterol >/=2.6 mmol/l
      [0.89 (95% CI 0.82-0.97)] and non-HDL cholesterol >/=3.1 mmol/l [0.85 (0.78 to
      0.93)] were significantly lower in the pump therapy group, even after all
      adjustments. CONCLUSIONS: Our results indicate that pump therapy is associated
      with a better lipid profile. This article is protected by copyright. All rights
      reserved.
CI  - This article is protected by copyright. All rights reserved.
FAU - Kosteria, I
AU  - Kosteria I
AD  - Diabetes Centre, Division of Endocrinology, Diabetes and Metabolism, First
      Department of Paediatrics, National and Kapodistrian University of Athens,
      Medical School, Aghia Sophia Children's Hospital, Athens, Greece.
FAU - Schwandt, A
AU  - Schwandt A
AD  - Institute of Epidemiology and Medical Biometry, ZIBMT, Ulm University, Ulm,
      Germany.
AD  - German Centre for Diabetes Research, Munich-Neuherberg, Germany.
FAU - Davis, E
AU  - Davis E
AD  - Centre for Child Health Research, Telethon Kids Institute, University of Western,
      Australia.
FAU - Jali, S
AU  - Jali S
AD  - J. N. Medical College (KAHER) and the KLE Diabetes Centre, KLES Dr Prabhakar Kore
      Hospital, Belgaum, India.
FAU - Prieto, M
AU  - Prieto M
AD  - Hospital de Pediatria Garrahan, Buenos Aires, Argentina.
FAU - Rottembourg, D
AU  - Rottembourg D
AD  - Faculty of Medicine and Health Sciences, Sherbrooke University, Sherbrooke,
      Canada.
CN  - SWEET study group
LA  - eng
PT  - Journal Article
DEP - 20190410
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
EDAT- 2019/04/12 06:00
MHDA- 2019/04/12 06:00
CRDT- 2019/04/12 06:00
PHST- 2019/04/12 06:00 [entrez]
PHST- 2019/04/12 06:00 [pubmed]
PHST- 2019/04/12 06:00 [medline]
AID - 10.1111/dme.13963 [doi]
PST - aheadofprint
SO  - Diabet Med. 2019 Apr 10. doi: 10.1111/dme.13963.

PMID- 30972797
OWN - NLM
STAT- Publisher
LR  - 20190411
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
DP  - 2019 Apr 10
TI  - Incidence and predictors of recurrent and other new diabetic foot ulcers: a
      retrospective cohort study.
LID - 10.1111/dme.13964 [doi]
AB  - AIMS: To estimate progression rates, evaluate risk factors for progression, and
      study rate ratios for progression among people with a healed diabetic foot ulcer 
      according to whether the healed ulcer was neuropathic, neuro-ischaemic or
      critically ischaemic. METHODS: We conducted a retrospective cohort study in all
      individuals with a healed diabetic foot ulcer treated at the Steno Diabetes
      Centre Copenhagen foot clinic in the period 2010 to 2016. The outcome of interest
      was recurrent/other new diabetic foot ulcers. RESULTS: A total of 780 people had 
      a healed diabetic foot ulcer in the study period (2010-2016). The participants
      were followed for 1249 person-years [median (Q1-Q3) 1.04 (0.38-2.46)
      person-years] in total. One-third (33.1%) developed a recurrent/other new
      diabetic foot ulcer per year. Male gender, people with Type 2 diabetes and
      smokers had a statistically significantly higher risk of progression to a
      recurrent/other new diabetic foot ulcer compared to participants without these
      risk factors. Participants with neuro-ischaemic or critically ischaemic diabetic 
      foot ulcers had statistically significantly higher progression rates than
      participants with neuropathic diabetic foot ulcers. CONCLUSIONS: Focus should be 
      on preventing future recurrent/other new diabetic foot ulcers especially in
      people with ischaemia. This article is protected by copyright. All rights
      reserved.
CI  - This article is protected by copyright. All rights reserved.
FAU - Engberg, S
AU  - Engberg S
AD  - Steno Diabetes Centre Copenhagen, Gentofte, Denmark.
FAU - Kirketerp-Moller, K
AU  - Kirketerp-Moller K
AD  - Steno Diabetes Centre Copenhagen, Gentofte, Denmark.
FAU - Andersen, H Ullits
AU  - Andersen HU
AD  - Steno Diabetes Centre Copenhagen, Gentofte, Denmark.
FAU - Rasmussen, A
AU  - Rasmussen A
AD  - Steno Diabetes Centre Copenhagen, Gentofte, Denmark.
LA  - eng
PT  - Journal Article
DEP - 20190410
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
EDAT- 2019/04/12 06:00
MHDA- 2019/04/12 06:00
CRDT- 2019/04/12 06:00
PHST- 2019/04/12 06:00 [entrez]
PHST- 2019/04/12 06:00 [pubmed]
PHST- 2019/04/12 06:00 [medline]
AID - 10.1111/dme.13964 [doi]
PST - aheadofprint
SO  - Diabet Med. 2019 Apr 10. doi: 10.1111/dme.13964.

PMID- 30972790
OWN - NLM
STAT- Publisher
LR  - 20190411
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
DP  - 2019 Apr 10
TI  - Risk factors and outcomes for neonatal hypoglycaemia and neonatal
      hyperbilirubinaemia in pregnancies complicated by gestational diabetes mellitus: 
      a single centre retrospective 3-year review.
LID - 10.1111/dme.13962 [doi]
AB  - AIM: To determine risk factors associated with neonatal hypoglycaemia and
      hyperbilirubinaemia, and assess their impact on neonatal outcomes in pregnancies 
      complicated by gestational diabetes mellitus (GDM). METHODS: Retrospective review
      investigating all pregnancies complicated by GDM at Campbelltown Hospital
      (Sydney, Australia) between 1 January 2013 and 31 December 2015. Main outcomes
      measured were neonatal hypoglycaemia (capillary glucose levels < 1.8 mmol/l) and 
      hyperbilirubinaemia (total serum bilirubin levels greater than age-appropriate
      thresholds for phototherapy). Adjusted odds ratios [95% confidence interval (CI)]
      are shown, calculated by multivariable logistic regression. RESULTS: Some 60
      (7.8%) infants developed hypoglycaemia, 58 (7.5%) developed hyperbilirubinaemia
      and 13 (1.7%) developed both. Risk of developing hypoglycaemia increased 1.8-fold
      (95% CI 1.3-2.6, P < 0.001) per gestational week at GDM diagnosis, 1.1-fold (95% 
      CI 1.0-1.3, P = 0.04) per mmol/l maternal fasting glucose, 6.2-fold (95% CI
      2.6-16.2, P < 0.001) with maternal history of macrosomia, 10.8-fold (95% CI
      4.1-27.6, P < 0.001) with multiple pregnancy and 1.1-fold (95% CI 1.0-1.3, P =
      0.04) per gestational week at birth. Risk of hyperbilirubinaemia increased with
      multiple pregnancy (26.4; 95% CI 11.7-59.7, P < 0.001), and 1.5-fold (95% CI
      1.1-2.1, P = 0.01) per gestational week at GDM diagnosis. Hypoglycaemia was
      associated with a 2.8-fold (95% CI 1.1-7.1, P = 0.03) increased risk of
      macrosomia, a 5.4-fold (95% CI 1.1-27.3, P = 0.04) excess risk of shoulder
      dystocia and a 6.4-fold increased risk of 5-min APGAR </= 7 (95% CI 1.2-1.7, P < 
      0.001). Hyperbilirubinaemia was associated with an excess risk of polycythaemia
      (packed cell volume > 0.6; 97.1, 95% CI 38.9-241.5, P < 0.001). CONCLUSIONS:
      Neonatal hypoglycaemia and hyperbilirubinaemia largely occur in different
      pregnancies. Both are associated with earlier GDM diagnosis; however,
      hypoglycaemia is more associated with maternal glycaemia and its sequelae, and
      hyperbilirubinaemia is associated with polycythaemia. This article is protected
      by copyright. All rights reserved.
CI  - This article is protected by copyright. All rights reserved.
FAU - Thevarajah, A
AU  - Thevarajah A
AD  - School of Medicine, Western Sydney University.
FAU - Simmons, D
AU  - Simmons D
AD  - School of Medicine, Western Sydney University.
AD  - Departmentt of Endocrinology, Campbelltown Hospital, Campbelltown, NSW,
      Australia.
LA  - eng
PT  - Journal Article
DEP - 20190410
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
EDAT- 2019/04/12 06:00
MHDA- 2019/04/12 06:00
CRDT- 2019/04/12 06:00
PHST- 2019/04/12 06:00 [entrez]
PHST- 2019/04/12 06:00 [pubmed]
PHST- 2019/04/12 06:00 [medline]
AID - 10.1111/dme.13962 [doi]
PST - aheadofprint
SO  - Diabet Med. 2019 Apr 10. doi: 10.1111/dme.13962.

PMID- 30955221
OWN - NLM
STAT- Publisher
LR  - 20190407
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
DP  - 2019 Apr 6
TI  - Persistent C-peptide is associated with reduced hypoglycaemia but not HbA1c in
      adults with longstanding Type 1 diabetes: evidence for lack of intensive
      treatment in UK clinical practice?
LID - 10.1111/dme.13960 [doi]
AB  - AIMS: Most people with Type 1 diabetes have low levels of persistent endogenous
      insulin production. The Diabetes Control and Complications Trial showed that
      close to diagnosis preserved endogenous insulin was associated with lower HbA1c ,
      hypoglycaemia and complication rates, when intensively treated. We aimed to
      assess the clinical impact of persistent C-peptide on rate of hypoglycaemia and
      HbA1c in those with long duration (> 5 years) Type 1 diabetes. METHODS: We
      conducted a cross-sectional case-control study of 221 people (median age 24
      years) with Type 1 diabetes. We confirmed ongoing endogenous insulin secretion by
      measuring C-peptide after a mixed-meal tolerance test. We compared self-reported 
      hypoglycaemia (n = 160), HbA1c , insulin dose and microvascular complications (n 
      = 140) in those with preserved and low C-peptide. RESULTS: Stimulated median
      (IQR) C-peptide was 114 (43, 273) pmol/l and < 3 (< 3, < 3) pmol/l in those with 
      preserved and low C-peptide respectively. Participants with preserved C-peptide
      had lower reported monthly rates of hypoglycaemia, with 21% fewer symptomatic
      episodes, 5.9 vs. 7.5 [incidence rate ratio (IRR) 0.79, P = 0.001], and 65% fewer
      asymptomatic episodes, 1.0 vs. 2.9 (IRR 0.35, P < 0.001). Those with preserved
      C-peptide had a lower insulin dose (0.68 vs. 0.81 units/kg, P = 0.01) but similar
      HbA1c (preserved 69 vs. low 67 mmol/mol, P = 0.06). CONCLUSIONS: Adults with Type
      1 diabetes and preserved endogenous insulin production receiving usual care in
      the UK have lower daily insulin doses and fewer self-reported hypoglycaemic
      episodes, but no difference in HbA1c . This is consistent with non-intensive
      treatment in previous studies, and suggests a need to consider therapy
      intensification to gain full benefit of preserved endogenous insulin. This
      article is protected by copyright. All rights reserved.
CI  - This article is protected by copyright. All rights reserved.
FAU - Marren, S M
AU  - Marren SM
AD  - Institute of Biomedical and Clinical Science, London, UK.
FAU - Hammersley, S
AU  - Hammersley S
AD  - NIHR Exeter Clinical Research Facility, University of Exeter Medical School,
      London, UK.
FAU - McDonald, T J
AU  - McDonald TJ
AD  - Institute of Biomedical and Clinical Science, London, UK.
AD  - NIHR Exeter Clinical Research Facility, University of Exeter Medical School,
      London, UK.
AD  - Blood Sciences, Royal Devon and Exeter NHS Foundation Trust, Exeter, London, UK.
FAU - Shields, B M
AU  - Shields BM
AD  - Institute of Biomedical and Clinical Science, London, UK.
AD  - NIHR Exeter Clinical Research Facility, University of Exeter Medical School,
      London, UK.
FAU - Knight, B
AU  - Knight B
AD  - NIHR Exeter Clinical Research Facility, University of Exeter Medical School,
      London, UK.
FAU - Hill, A
AU  - Hill A
AD  - NIHR Exeter Clinical Research Facility, University of Exeter Medical School,
      London, UK.
FAU - Bolt, R
AU  - Bolt R
AD  - NIHR Exeter Clinical Research Facility, University of Exeter Medical School,
      London, UK.
FAU - Tree, T
AU  - Tree T
AD  - Department of Immunobiology, School of Immunobiology & Microbial Sciences, Kings 
      College London, London, UK.
AD  - NIHR Biomedical Research Centre Guys and St Thomas' NHS Foundation Trust and
      Kings College London, London, UK.
FAU - Roep, B
AU  - Roep B
AD  - Department of Diabetes Immunology, Diabetes& Metabolism Research Institute at the
      City of Hope National Medical Center,, Duarte, CA, USA.
AD  - Department of Immunohaematology & Blood Transfusion, Leiden University Medical
      Center, Leiden, The Netherlands.
FAU - Hattersley, A T
AU  - Hattersley AT
AD  - Institute of Biomedical and Clinical Science, London, UK.
AD  - NIHR Exeter Clinical Research Facility, University of Exeter Medical School,
      London, UK.
FAU - Jones, A G
AU  - Jones AG
AD  - Institute of Biomedical and Clinical Science, London, UK.
AD  - NIHR Exeter Clinical Research Facility, University of Exeter Medical School,
      London, UK.
FAU - Oram, R A
AU  - Oram RA
AD  - Institute of Biomedical and Clinical Science, London, UK.
AD  - NIHR Exeter Clinical Research Facility, University of Exeter Medical School,
      London, UK.
CN  - TIGI consortium
LA  - eng
PT  - Journal Article
DEP - 20190406
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
EDAT- 2019/04/08 06:00
MHDA- 2019/04/08 06:00
CRDT- 2019/04/08 06:00
PHST- 2019/04/08 06:00 [entrez]
PHST- 2019/04/08 06:00 [pubmed]
PHST- 2019/04/08 06:00 [medline]
AID - 10.1111/dme.13960 [doi]
PST - aheadofprint
SO  - Diabet Med. 2019 Apr 6. doi: 10.1111/dme.13960.

PMID- 30967424
OWN - NLM
STAT- Publisher
LR  - 20190417
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2019 Apr 9
TI  - Low-dose Anti-Thymocyte Globulin Preserves C-Peptide and Reduces A1c in New Onset
      Type 1 Diabetes: Two Year Clinical Trial Data.
LID - db190057 [pii]
LID - 10.2337/db19-0057 [doi]
AB  - A three-arm, randomized, double-masked, placebo-controlled phase 2b trial
      performed by the Type 1 Diabetes TrialNet Study Group previously demonstrated
      that low-dose anti-thymocyte globulin (ATG, 2.5mg/kg) preserved beta-cell
      function and reduced HbA1c for one year in new-onset type 1 diabetes. Subjects
      (N=89) were randomized to: 1) ATG and pegylated granulocyte-colony stimulating
      factor (GCSF); 2) ATG alone; or 3) placebo. Herein, we report two-year AUC
      C-peptide and HbA1c, pre-specified secondary endpoints, and potential immunologic
      correlates. The two-year mean mixed-meal tolerance test (MMTT)-stimulated AUC
      C-peptide, analyzed by ANCOVA adjusting for baseline C-peptide, age, and sex
      (N=82) with significance defined as one-sided p<0.025, was significantly higher
      in subjects treated with ATG versus placebo (p=0.00005) but not ATG/GCSF versus
      placebo (p=0.032). HbA1c was significantly reduced at 2-years in subjects treated
      with ATG (p=0.011) and ATG/GCSF (p=0.022) versus placebo. Flow-cytometric
      analyses demonstrated reduced circulating CD4:CD8 ratio, increased regulatory T
      cell (Treg): conventional CD4 T cell (Tconv) ratios, and increased PD-1(+)CD4(+) 
      T cells following low-dose ATG and ATG/GCSF. Low-dose ATG partially preserved
      beta-cell function and reduced HbA1c two years after therapy in new-onset type 1 
      diabetes. Future studies should determine whether low-dose ATG might prevent or
      delay the onset of type 1 diabetes.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Haller, Michael J
AU  - Haller MJ
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
      hallemj@peds.ufl.edu.
FAU - Long, S Alice
AU  - Long SA
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Blanchfield, J Lori
AU  - Blanchfield JL
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Schatz, Desmond A
AU  - Schatz DA
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Skyler, Jay S
AU  - Skyler JS
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Krischer, Jeffrey P
AU  - Krischer JP
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Bundy, Brian N
AU  - Bundy BN
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Geyer, Susan M
AU  - Geyer SM
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Warnock, Megan V
AU  - Warnock MV
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Miller, Jessica L
AU  - Miller JL
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Atkinson, Mark A
AU  - Atkinson MA
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Becker, Dorothy J
AU  - Becker DJ
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Baidal, David A
AU  - Baidal DA
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - DiMeglio, Linda A
AU  - DiMeglio LA
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Gitelman, Stephen E
AU  - Gitelman SE
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Goland, Robin
AU  - Goland R
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Gottlieb, Peter A
AU  - Gottlieb PA
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Herold, Kevan C
AU  - Herold KC
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Marks, Jennifer B
AU  - Marks JB
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Moran, Antoinette
AU  - Moran A
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Rodriguez, Henry
AU  - Rodriguez H
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Russell, William E
AU  - Russell WE
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Wilson, Darrell M
AU  - Wilson DM
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
FAU - Greenbaum, Carla J
AU  - Greenbaum CJ
AD  - From the University of Florida Diabetes Institute, Gainesville, FL (M.J.H.,
      D.A.S. M.A.A.), Benaroya Research Institute, Seattle, WA (S.A.L, L.B. and C.J.G),
      Diabetes Research Institute, University of Miami Miller School of Medicine,
      Miami, FL, (J.S.S., D.B., J.B.M.), University of South Florida, Tampa, FL (J.P.K,
      B.N.B., S.M.G., M.W., J.L.M., H.R.), University of Pittsburgh, Pittsburgh, PA
      (D.J.B.), Indiana University, Indianapolis, IN (L.A.D.), University of California
      San Francisco, San Francisco, CA (S.E.G.), Columbia University, New York, NY
      (R.G.), University of Colorado Barbara Davis Center for Childhood Diabetes,
      Aurora, CO, (P.A.G.), Yale University, New Haven, CT (K.C.H.), University of
      Minnesota, Minneapolis, MN, (A.M.), Vanderbilt University, Nashville, TN
      (W.E.R.), The National Institute of Diabetes and Digestive and Kidney Diseases,
      Bethesda, MD (L.M.S.), and Stanford University, Stanford, CA (D.M.W.).
CN  - Type 1 Diabetes TrialNet ATG-GCSF Study Group
LA  - eng
GR  - P01 AI042288/AI/NIAID NIH HHS/United States
PT  - Journal Article
DEP - 20190409
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
EDAT- 2019/04/11 06:00
MHDA- 2019/04/11 06:00
CRDT- 2019/04/11 06:00
PHST- 2019/01/17 00:00 [received]
PHST- 2019/03/23 00:00 [accepted]
PHST- 2019/04/11 06:00 [entrez]
PHST- 2019/04/11 06:00 [pubmed]
PHST- 2019/04/11 06:00 [medline]
AID - db19-0057 [pii]
AID - 10.2337/db19-0057 [doi]
PST - aheadofprint
SO  - Diabetes. 2019 Apr 9. pii: db19-0057. doi: 10.2337/db19-0057.

PMID- 30962220
OWN - NLM
STAT- Publisher
LR  - 20190409
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2019 Apr 8
TI  - Trisomy 21 is a Cause of Permanent Neonatal Diabetes that is Autoimmune but not
      HLA Associated.
LID - db190045 [pii]
LID - 10.2337/db19-0045 [doi]
AB  - Identifying new causes of permanent neonatal diabetes (diagnosis <6 months; PNDM)
      provides important insights into beta-cell biology. Patients with Down syndrome
      (DS) resulting from trisomy 21 are 4 times more likely to have childhood diabetes
      with an intermediate HLA association. It is not known if DS can cause PNDM. We
      found trisomy 21 was 7 times more likely in our PNDM cohort than in the
      population (13/1522 = 85/10,000 observed vs. 12.6/10,000 expected) and none of
      the 13 DS-PNDM cases had a mutation in the known PNDM genes which explained 82.9%
      of non-DS PNDM. Islet autoantibodies were present in 4/9 DS-PNDM patients but
      DS-PNDM was not associated with polygenic susceptibility to type 1 diabetes. We
      conclude that trisomy 21 is a cause of autoimmune PNDM that is not HLA
      associated. We propose that autoimmune diabetes in DS is heterogeneous and
      includes coincidental type 1 diabetes that is HLA associated and diabetes caused 
      by trisomy 21 that is not HLA associated.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Johnson, Matthew B
AU  - Johnson MB
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical
      School, Exeter, UK.
FAU - De Franco, Elisa
AU  - De Franco E
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical
      School, Exeter, UK.
FAU - Atma W Greeley, Siri
AU  - Atma W Greeley S
AD  - Section of Adult and Pediatric Endocrinology, Diabetes and Metabolism, Kovler
      Diabetes Center, The University of Chicago, Chicago, IL, USA.
FAU - Letourneau, Lisa R
AU  - Letourneau LR
AD  - Section of Adult and Pediatric Endocrinology, Diabetes and Metabolism, Kovler
      Diabetes Center, The University of Chicago, Chicago, IL, USA.
FAU - Gillespie, Kathleen
AU  - Gillespie K
AD  - Bristol Medical School, University of Bristol, Bristol, U.K.
CN  - International DS-PNDM consortium
FAU - Wakeling, Matthew N
AU  - Wakeling MN
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical
      School, Exeter, UK.
FAU - Ellard, Sian
AU  - Ellard S
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical
      School, Exeter, UK.
FAU - Flanagan, Sarah E
AU  - Flanagan SE
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical
      School, Exeter, UK.
FAU - Patel, Kashyap A
AU  - Patel KA
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical
      School, Exeter, UK.
FAU - Hattersley, Andrew T
AU  - Hattersley AT
AD  - Institute of Biomedical and Clinical Science, University of Exeter Medical
      School, Exeter, UK A.T.Hattersley@exeter.ac.uk.
LA  - eng
PT  - Journal Article
DEP - 20190408
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
EDAT- 2019/04/10 06:00
MHDA- 2019/04/10 06:00
CRDT- 2019/04/10 06:00
PHST- 2019/01/15 00:00 [received]
PHST- 2019/03/27 00:00 [accepted]
PHST- 2019/04/10 06:00 [entrez]
PHST- 2019/04/10 06:00 [pubmed]
PHST- 2019/04/10 06:00 [medline]
AID - db19-0045 [pii]
AID - 10.2337/db19-0045 [doi]
PST - aheadofprint
SO  - Diabetes. 2019 Apr 8. pii: db19-0045. doi: 10.2337/db19-0045.

PMID- 30962219
OWN - NLM
STAT- Publisher
LR  - 20190409
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2019 Apr 8
TI  - Genetic Variation Within the HLA-DRA1 Gene Modulates Susceptibility to Type 1
      Diabetes in HLA-DR3 Homozygotes.
LID - db181128 [pii]
LID - 10.2337/db18-1128 [doi]
AB  - Type 1 diabetes (T1D) involves the interaction of multiple gene variants,
      environmental factors, and immunoregulatory dysfunction. Major T1D genetic risk
      loci T1D encode the Human Leukocyte Antigens HLA-DR and DQ. Genetic heterogeneity
      and linkage disequilibrium in the highly polymorphic HLA region confound attempts
      to identify additional T1D susceptibility loci. To minimize HLA heterogeneity,
      T1D patients (N=365) and controls (N=668) homozygous for the HLA-DR3 high-risk
      haplotype were selected from multiple large T1D studies and examined to identify 
      new T1D susceptibility loci using molecular inversion probe sequencing
      technology. We report that risk for T1D in HLA-DR3 homozygotes is increased
      significantly by a previously unreported haplotype of three SNPs within the first
      intron of HLA-DRA1. The homozygous risk haplotype has an odds ratio of 4.65
      relative to the protective homozygous haplotype in our sample. Individually,
      these SNPs reportedly function as "expression quantitative trait loci,"
      modulating HLA-DR and DQ expression. Analysis of available data concludes that
      the tri-SNP haplotype within HLA-DRA1 may modulate class II expression,
      suggesting that increased T1D risk could be attributable to regulated expression 
      of class II genes. These findings could help clarify the role of HLA in T1D
      susceptibility and improve diabetes risk assessment, particularly in high-risk
      HLA-DR3 homozygous individuals.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Aydemir, Ozkan
AU  - Aydemir O
AD  - Department of Medicine, Divisions of Transfusion Medicine, University of
      Massachusetts Medical School, Worcester, MA.
FAU - Noble, Janelle A
AU  - Noble JA
AD  - Children's Hospital Oakland Research Institute, Oakland, CA.
FAU - Bailey, Jeffrey
AU  - Bailey J
AD  - Department of Medicine, Divisions of Transfusion Medicine, University of
      Massachusetts Medical School, Worcester, MA.
FAU - Lernmark, Ake
AU  - Lernmark A
AD  - Department of Clinical Sciences, Lund University/CRC, Skane University Hospital, 
      Malmo, Sweden.
FAU - Marsh, Patrick
AU  - Marsh P
AD  - Department of Medicine, Divisions of Transfusion Medicine, University of
      Massachusetts Medical School, Worcester, MA.
FAU - Svard, Agnes Andersson
AU  - Svard AA
AD  - Department of Clinical Sciences, Lund University/CRC, Skane University Hospital, 
      Malmo, Sweden.
FAU - Bearoff, Frank
AU  - Bearoff F
AD  - Department of Microbiology and Immunology, Drexel University College of Medicine,
      Philadelphia, PA.
FAU - Blankenhorn, Elizabeth P
AU  - Blankenhorn EP
AD  - Department of Microbiology and Immunology, Drexel University College of Medicine,
      Philadelphia, PA.
FAU - Mordes, John P
AU  - Mordes JP
AD  - Department of Medicine and Endocrinology, University of Massachusetts Medical
      School, Worcester, MA John.Mordes@umassmed.edu.
CN  - Better Diabetes Diagnosis (BDD) Study Group
LA  - eng
PT  - Journal Article
DEP - 20190408
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
EDAT- 2019/04/10 06:00
MHDA- 2019/04/10 06:00
CRDT- 2019/04/10 06:00
PHST- 2018/10/17 00:00 [received]
PHST- 2019/03/28 00:00 [accepted]
PHST- 2019/04/10 06:00 [entrez]
PHST- 2019/04/10 06:00 [pubmed]
PHST- 2019/04/10 06:00 [medline]
AID - db18-1128 [pii]
AID - 10.2337/db18-1128 [doi]
PST - aheadofprint
SO  - Diabetes. 2019 Apr 8. pii: db18-1128. doi: 10.2337/db18-1128.

PMID- 30967437
OWN - NLM
STAT- Publisher
LR  - 20190410
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Apr 9
TI  - Diabetes-Related Complications and Mortality in Patients With Young-Onset Latent 
      Autoimmune Diabetes: A 14-Year Analysis of the Prospective Hong Kong Diabetes
      Register.
LID - dc181796 [pii]
LID - 10.2337/dc18-1796 [doi]
AB  - OBJECTIVE: Young-onset diabetes is heterogeneous in etiology and disease
      progression. We compared the incidence of diabetes-related complications and
      mortality in patients with young-onset type 2 diabetes with or without anti-GAD
      antibodies and patients with type 1 diabetes. We determined changes in glycemic
      control before and after commencement of insulin therapy stratified by antibody
      status. RESEARCH DESIGN AND METHODS: Between 1994 and 2012, 1,504 consecutively
      enrolled patients with type 2 diabetes who had received a diagnosis at <40 years 
      of age and had available anti-GAD antibody status, and 251 patients with type 1
      diabetes from the Hong Kong Diabetes Register were followed for incident
      cardiovascular disease (CVD), end-stage renal disease (ESRD), severe
      hypoglycemia, and all-cause mortality until June 2015. Information on insulin use
      and HbA1c levels during follow-up was obtained. RESULTS: Anti-GAD antibodies were
      positive in 8.1% of patients with type 2 diabetes (GAD(+)). Using multivariate
      Cox regression, patients with GAD(+) had a lower hazard of CVD (hazard ratio [HR]
      0.43, P = 0.048), a higher hazard of severe hypoglycemia (HR 1.63, P = 0.032),
      and a similar hazard of ESRD and mortality compared with counterparts without
      anti-GAD antibodies (GAD(-)). Compared with patients with type 1 diabetes, ESRD
      were more likely to develop (HR 2.91, P = 0.043) in patients with GAD(+), but no 
      differences were detected in the hazards of severe hypoglycemia, CVD, and
      mortality. Among new insulin users (n = 304), patients with GAD(+) had larger
      reductions in HbA1c than patients with GAD(-)after 12 months of insulin use
      (-2.30 +/- 3.80% [25 +/- 42 mmol/mol] vs -0.72 +/- 1.86% [8 +/- 20 mmol/mol], P =
      0.05). CONCLUSIONS: Anti-GAD positivity identifies a group of patients with a
      different prognosis compared with patients without antibodies and those with type
      1 diabetes. Patients with GAD(+) responded differently to insulin compared with
      patients with GAD(-).
CI  - (c) 2019 by the American Diabetes Association.
FAU - Luk, Andrea O Y
AU  - Luk AOY
AUID- ORCID: http://orcid.org/0000-0002-5244-6069
AD  - Department of Medicine and Therapeutics, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China
      andrealuk@cuhk.edu.hk.
AD  - Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
AD  - Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
FAU - Lau, Eric S H
AU  - Lau ESH
AD  - Asia Diabetes Foundation, Hong Kong Special Administrative Region, People's
      Republic of China.
FAU - Lim, Cadmon
AU  - Lim C
AD  - Department of Medicine and Therapeutics, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
FAU - Kong, Alice P S
AU  - Kong APS
AUID- ORCID: http://orcid.org/0000-0001-8927-6764
AD  - Department of Medicine and Therapeutics, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
AD  - Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
AD  - Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
FAU - Chow, Elaine
AU  - Chow E
AD  - Department of Medicine and Therapeutics, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
FAU - Ma, Ronald C W
AU  - Ma RCW
AUID- ORCID: http://orcid.org/0000-0002-1227-803X
AD  - Department of Medicine and Therapeutics, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
AD  - Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
AD  - Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
FAU - Chan, Juliana C N
AU  - Chan JCN
AUID- ORCID: http://orcid.org/0000-0003-1325-1194
AD  - Department of Medicine and Therapeutics, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
AD  - Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
AD  - Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong,
      Hong Kong Special Administrative Region, People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20190409
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/04/11 06:00
MHDA- 2019/04/11 06:00
CRDT- 2019/04/11 06:00
PHST- 2018/08/24 00:00 [received]
PHST- 2019/03/12 00:00 [accepted]
PHST- 2019/04/11 06:00 [entrez]
PHST- 2019/04/11 06:00 [pubmed]
PHST- 2019/04/11 06:00 [medline]
AID - dc18-1796 [pii]
AID - 10.2337/dc18-1796 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Apr 9. pii: dc18-1796. doi: 10.2337/dc18-1796.

PMID- 30967436
OWN - NLM
STAT- Publisher
LR  - 20190410
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Apr 9
TI  - Efficacy of Fish Oil and/or Probiotic Intervention on the Incidence of
      Gestational Diabetes Mellitus in an At-Risk Group of Overweight and Obese Women: 
      A Randomized, Placebo-Controlled, Double-Blind Clinical Trial.
LID - dc182591 [pii]
LID - 10.2337/dc18-2591 [doi]
AB  - OBJECTIVE: To assess whether the risk of gestational diabetes mellitus (GDM) may 
      be lowered and glucose metabolism improved by daily administration of fish oil
      and/or probiotic supplements in overweight and obese pregnant women. RESEARCH
      DESIGN AND METHODS: We randomized in a double-blind manner 439 women (mean 13.9
      +/- 2.1 gestational weeks [gw]) into four intervention groups: fish oil +
      placebo, probiotics + placebo, fish oil + probiotics, and placebo + placebo. Fish
      oil (1.9 g docosahexaenoic acid and 0.22 g eicosapentaenoic acid) and probiotic
      supplements (Lactobacillus rhamnosus HN001 and Bifidobacterium animalis ssp.
      lactis 420, 10(10) colony-forming units each) were provided for daily consumption
      from randomization beyond delivery. Primary outcomes were the incidence of GDM
      diagnosed with oral glucose tolerance test targeted at 24-28 gw and the change in
      fasting glucose between randomization and late pregnancy (mean 35.2 +/- 0.9 gw). 
      Insulin concentration, insulin resistance HOMA2-IR index, and pregnancy outcomes 
      were determined, as were adverse effects related to the intervention. Analyses
      were by intent to treat. RESULTS: No differences were found among the
      intervention groups in the maternal and neonatal pregnancy outcomes or side
      effects related to the intervention (P > 0.05). The proportion of women with GDM 
      (94 of 377; fish oil + placebo, 23 of 96, 24.0%; probiotics + placebo, 25 of 99, 
      25.3%; fish oil + probiotics, 26 of 91, 28.6%; and placebo + placebo, 20 of 91,
      22.0%) or the change in glucose, insulin, or HOMA2-IR (n = 364) did not differ
      among the intervention groups (P > 0.11 for all comparisons). CONCLUSIONS: An
      intervention with fish oil and/or probiotics during pregnancy seemed to be both
      safe and well tolerated but conferred no benefits in lowering the risk of GDM or 
      improving glucose metabolism in overweight and obese women.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Pellonpera, Outi
AU  - Pellonpera O
AUID- ORCID: http://orcid.org/0000-0001-9272-2278
AD  - Department of Obstetrics and Gynecology, University of Turku and Turku University
      Hospital, Turku, Finland outi.pellonpera@utu.fi.
FAU - Mokkala, Kati
AU  - Mokkala K
AUID- ORCID: http://orcid.org/0000-0002-0354-5546
AD  - Institute of Biomedicine, Integrative Physiology, and Pharmacology, University of
      Turku, Turku, Finland.
FAU - Houttu, Noora
AU  - Houttu N
AD  - Institute of Biomedicine, Integrative Physiology, and Pharmacology, University of
      Turku, Turku, Finland.
FAU - Vahlberg, Tero
AU  - Vahlberg T
AD  - Institute of Clinical Medicine, Biostatistics, University of Turku, Turku,
      Finland.
FAU - Koivuniemi, Ella
AU  - Koivuniemi E
AD  - Institute of Biomedicine, Integrative Physiology, and Pharmacology, University of
      Turku, Turku, Finland.
FAU - Tertti, Kristiina
AU  - Tertti K
AD  - Department of Obstetrics and Gynecology, University of Turku and Turku University
      Hospital, Turku, Finland.
FAU - Ronnemaa, Tapani
AU  - Ronnemaa T
AD  - Department of Medicine, University of Turku and Turku University Hospital, Turku,
      Finland.
FAU - Laitinen, Kirsi
AU  - Laitinen K
AUID- ORCID: http://orcid.org/0000-0001-5245-8118
AD  - Institute of Biomedicine, Integrative Physiology, and Pharmacology, University of
      Turku, Turku, Finland.
LA  - eng
PT  - Journal Article
DEP - 20190409
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/04/11 06:00
MHDA- 2019/04/11 06:00
CRDT- 2019/04/11 06:00
PHST- 2018/12/18 00:00 [received]
PHST- 2019/02/27 00:00 [accepted]
PHST- 2019/04/11 06:00 [entrez]
PHST- 2019/04/11 06:00 [pubmed]
PHST- 2019/04/11 06:00 [medline]
AID - dc18-2591 [pii]
AID - 10.2337/dc18-2591 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Apr 9. pii: dc18-2591. doi: 10.2337/dc18-2591.

PMID- 30967435
OWN - NLM
STAT- Publisher
LR  - 20190410
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Apr 9
TI  - Elevated Serum Uric Acid Is Associated With Greater Risk for Hypertension and
      Diabetic Kidney Diseases in Obese Adolescents With Type 2 Diabetes: An
      Observational Analysis From the Treatment Options for Type 2 Diabetes in
      Adolescents and Youth (TODAY) Study.
LID - dc182147 [pii]
LID - 10.2337/dc18-2147 [doi]
AB  - OBJECTIVE: Elevated serum uric acid (SUA) is increasingly recognized as a risk
      factor for kidney disease in adults with diabetes, but data in youth are limited.
      We hypothesized that elevated SUA predicts development of elevated urinary
      albumin excretion (UAE) and hypertension over time in teens with type 2 diabetes 
      (T2D). RESEARCH DESIGN AND METHODS: Serum creatinine, cystatin C, SUA, and the
      urine albumin-to-creatinine ratio (UACR) were assessed in 539 obese youth, ages
      12-17 years, with T2D duration <2 years at baseline in the Treatment Options for 
      Type 2 Diabetes in Adolescents and Youth (TODAY) study. Estimated glomerular
      filtration rate (eGFR) was calculated using creatinine and cystatin C.
      Hypertension was defined as systolic or diastolic blood pressure >/=130/80 mmHg
      and elevated urine albumin excretion (UAE) as UACR >/=30 mg/g. Cox proportional
      hazard models evaluated the relationship between SUA and outcome variables
      longitudinally over an average follow-up of 5.7 years, adjusting for age, sex,
      race/ethnicity, BMI, HbA1c, eGFR, ACE inhibitor/angiotensin receptor blocker use,
      and TODAY treatment group assignment. RESULTS: At baseline, hyperuricemia (>/=6.8
      mg/dL) was present in 25.6% of participants, hypertension in 18.7%, and elevated 
      UAE in 6.1%. During follow-up of up to 7 years, hypertension developed in 37.4%
      and UAE in 18.0%. Higher baseline SUA increased the risk of incident hypertension
      (hazard ratio [HR] 1.19, 95% CI 1.03-1.38, per 1 mg/dL increase in SUA) and
      elevated UAE (HR 1.24, 95% CI 1.03-1.48) in adjusted models. CONCLUSIONS:
      Hyperuricemia was common in youth with T2D. Higher baseline SUA independently
      increased the risk for onset of hypertension and elevated UAE. Research is needed
      to determine whether SUA-lowering therapies can impede development of diabetic
      kidney disease and hypertension in T2D youth.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Bjornstad, Petter
AU  - Bjornstad P
AUID- ORCID: http://orcid.org/0000-0002-5160-2947
AD  - University of Colorado Anschutz Medical Campus and Children's Hospital Colorado, 
      Aurora, CO.
FAU - Laffel, Lori
AU  - Laffel L
AUID- ORCID: http://orcid.org/0000-0002-9675-3001
AD  - Joslin Diabetes Center, Boston, MA.
FAU - Lynch, Jane
AU  - Lynch J
AD  - The University of Texas Health Science Center at San Antonio, San Antonio, TX.
FAU - El Ghormli, Laure
AU  - El Ghormli L
AUID- ORCID: http://orcid.org/0000-0003-4223-8407
AD  - George Washington University Biostatistics Center, Rockville, MD
      elghorml@bsc.gwu.edu.
FAU - Weinstock, Ruth S
AU  - Weinstock RS
AD  - Department of Medicine, State University of New York Upstate Medical University, 
      Syracuse, NY.
FAU - Tollefsen, Sherida E
AU  - Tollefsen SE
AD  - Department of Pediatrics, Saint Louis University Health Sciences Center, St.
      Louis, MO.
FAU - Nadeau, Kristen J
AU  - Nadeau KJ
AD  - University of Colorado Anschutz Medical Campus and Children's Hospital Colorado, 
      Aurora, CO.
CN  - TODAY Study Group*
LA  - eng
PT  - Journal Article
DEP - 20190409
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/04/11 06:00
MHDA- 2019/04/11 06:00
CRDT- 2019/04/11 06:00
PHST- 2018/10/12 00:00 [received]
PHST- 2019/03/12 00:00 [accepted]
PHST- 2019/04/11 06:00 [entrez]
PHST- 2019/04/11 06:00 [pubmed]
PHST- 2019/04/11 06:00 [medline]
AID - dc18-2147 [pii]
AID - 10.2337/dc18-2147 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Apr 9. pii: dc18-2147. doi: 10.2337/dc18-2147.

PMID- 30967434
OWN - NLM
STAT- Publisher
LR  - 20190410
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Apr 9
TI  - Glucose Variables in Type 1 Diabetes Studies With Dapagliflozin: Pooled Analysis 
      of Continuous Glucose Monitoring Data From DEPICT-1 and -2.
LID - dc181983 [pii]
LID - 10.2337/dc18-1983 [doi]
AB  - OBJECTIVE: This pooled analysis assessed continuous glucose monitoring (CGM) in
      patients with inadequately controlled type 1 diabetes (HbA1c >/=7.7 to </=11.0%
      [>/=61 to </=97 mmol/mol]) who received dapagliflozin as an adjunct to adjustable
      insulin. RESEARCH DESIGN AND METHODS: CGM data were pooled from two 24-week,
      double-blind, randomized, phase 3 studies: Dapagliflozin Evaluation in Patients
      with Inadequately Controlled Type 1 diabetes (DEPICT-1 and DEPICT-2). These
      studies comprised 1,591 patients receiving dapagliflozin 5 mg (n = 530),
      dapagliflozin 10 mg (n = 529), or placebo (n = 532). RESULTS: Baseline
      characteristics were balanced between treatment groups. Patients receiving
      dapagliflozin 5 mg or 10 mg both spent more time with HbA1c in the range of >3.9 
      to </=10.0 mmol/L (>70 to </=180 mg/dL) over 24 h than those receiving the
      placebo. The adjusted mean (SE) change from baseline at week 24 was 6.48% (0.60) 
      with dapagliflozin 5 mg, 8.08% (0.60) with dapagliflozin 10 mg, and -2.59% (0.61)
      with placebo. At week 24, the mean amplitude of glucose excursion over 24 h, mean
      24-h glucose values, and postprandial glucose values were also improved in
      patients receiving dapagliflozin over those receiving placebo. No marked
      differences were found at week 24 between dapagliflozin 5 or 10 mg and placebo
      with regard to the percentage of glucose values </=3.9 mmol/L (</=70 mg/dL) or
      </=3.0 mmol/L (</=54 mg/dL) over 24 h, or to nocturnal (0000-0559 h) glucose
      values </=3.9 mmol/L (</=70 mg/dL). CONCLUSIONS: In patients with type 1
      diabetes, treatment with dapagliflozin over 24 weeks improved time in range, mean
      glucose, and glycemic variability without increasing the time spent in the range 
      indicating hypoglycemia.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Mathieu, Chantal
AU  - Mathieu C
AUID- ORCID: http://orcid.org/0000-0002-6099-2406
AD  - Clinical and Experimental Endocrinology, University of Leuven, Leuven, Belgium
      chantal.mathieu@uzleuven.be.
FAU - Dandona, Paresh
AU  - Dandona P
AUID- ORCID: http://orcid.org/0000-0002-7055-2084
AD  - Department of Medicine, State University of New York at Buffalo, Buffalo, NY.
FAU - Phillip, Moshe
AU  - Phillip M
AD  - Institute for Endocrinology & Diabetes, Schneider Children's Medical Centre of
      Israel, Petah Tikva, Israel.
AD  - Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
FAU - Oron, Tal
AU  - Oron T
AD  - Institute for Endocrinology & Diabetes, Schneider Children's Medical Centre of
      Israel, Petah Tikva, Israel.
AD  - Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
FAU - Lind, Marcus
AU  - Lind M
AUID- ORCID: http://orcid.org/0000-0002-3796-9283
AD  - Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.
AD  - Department of Medicine, NU Hospital Group, Uddevalla, Sweden.
FAU - Hansen, Lars
AU  - Hansen L
AD  - MedImmune, Gaithersburg, MD.
FAU - Thoren, Fredrik
AU  - Thoren F
AD  - AstraZeneca, Molndal, Sweden.
FAU - Xu, John
AU  - Xu J
AD  - AstraZeneca, Gaithersburg, MD.
FAU - Langkilde, Anna Maria
AU  - Langkilde AM
AD  - AstraZeneca, Molndal, Sweden.
CN  - DEPICT-1 and DEPICT-2 Investigators
LA  - eng
PT  - Journal Article
DEP - 20190409
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/04/11 06:00
MHDA- 2019/04/11 06:00
CRDT- 2019/04/11 06:00
PHST- 2018/09/19 00:00 [received]
PHST- 2019/03/08 00:00 [accepted]
PHST- 2019/04/11 06:00 [entrez]
PHST- 2019/04/11 06:00 [pubmed]
PHST- 2019/04/11 06:00 [medline]
AID - dc18-1983 [pii]
AID - 10.2337/dc18-1983 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Apr 9. pii: dc18-1983. doi: 10.2337/dc18-1983.

PMID- 30967432
OWN - NLM
STAT- Publisher
LR  - 20190410
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Apr 9
TI  - Predicting Islet Cell Autoimmunity and Type 1 Diabetes: An 8-Year TEDDY Study
      Progress Report.
LID - dc182282 [pii]
LID - 10.2337/dc18-2282 [doi]
AB  - OBJECTIVE: Assessment of the predictive power of TEDDY-identified risk factors
      for islet autoimmunity (IA), the type of autoantibody appearing first, and type 1
      diabetes (T1D). RESEARCH DESIGN AND METHODS: A total of 7,777 children were
      followed from birth to a median of 9.1 years of age for the development of islet 
      autoantibodies and progression to T1D. Time-dependent sensitivity, specificity,
      and receiver operating characteristic (ROC) curves were calculated to provide
      estimates of their individual and collective ability to predict IA and T1D.
      RESULTS: HLA genotype (DR3/4 vs. others) was the best predictor for IA (Youden's 
      index J = 0.117) and single nucleotide polymorphism rs2476601, in PTPN22, was the
      best predictor for insulin autoantibodies (IAA) appearing first (IAA-first) (J = 
      0.123). For GAD autoantibodies (GADA)-first, weight at 1 year was the best
      predictor (J = 0.114). In a multivariate model, the area under the ROC curve
      (AUC) was 0.678 (95% CI 0.655, 0.701), 0.707 (95% CI 0.676, 0.739), and 0.686
      (95% CI 0.651, 0.722) for IA, IAA-first, and GADA-first, respectively, at 6
      years. The AUC of the prediction model for T1D at 3 years after the appearance of
      multiple autoantibodies reached 0.706 (95% CI 0.649, 0.762). CONCLUSIONS:
      Prediction modeling statistics are valuable tools, when applied in a
      time-until-event setting, to evaluate the ability of risk factors to discriminate
      between those who will and those who will not get disease. Although significantly
      associated with IA and T1D, the TEDDY risk factors individually contribute little
      to prediction. However, in combination, these factors increased IA and T1D
      prediction substantially.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Krischer, Jeffrey P
AU  - Krischer JP
AUID- ORCID: http://orcid.org/0000-0003-4526-888X
FAU - Liu, Xiang
AU  - Liu X
FAU - Vehik, Kendra
AU  - Vehik K
FAU - Akolkar, Beena
AU  - Akolkar B
FAU - Hagopian, William A
AU  - Hagopian WA
FAU - Rewers, Marian J
AU  - Rewers MJ
FAU - She, Jin-Xiong
AU  - She JX
FAU - Toppari, Jorma
AU  - Toppari J
FAU - Ziegler, Anette G
AU  - Ziegler AG
AUID- ORCID: http://orcid.org/0000-0002-6290-5548
FAU - Lernmark, Ake
AU  - Lernmark A
CN  - TEDDY Study Group
LA  - eng
PT  - Journal Article
DEP - 20190409
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
IR  - Rewers M
FIR - Rewers, Marian
IR  - Bautista K
FIR - Bautista, Kimberly
IR  - Baxter J
FIR - Baxter, Judith
IR  - Felipe-Morales D
FIR - Felipe-Morales, Daniel
IR  - Driscoll K
FIR - Driscoll, Kimberly
IR  - Frohnert BI
FIR - Frohnert, Brigitte I
IR  - Gallant M
FIR - Gallant, Marisa
IR  - Gesualdo P
FIR - Gesualdo, Patricia
IR  - Hoffman M
FIR - Hoffman, Michelle
IR  - Karban R
FIR - Karban, Rachel
IR  - Liu E
FIR - Liu, Edwin
IR  - Norris J
FIR - Norris, Jill
IR  - Steck A
FIR - Steck, Andrea
IR  - Waugh K
FIR - Waugh, Kathleen
IR  - Toppari J
FIR - Toppari, Jorma
IR  - Simell OG
FIR - Simell, Olli G
IR  - Adamsson A
FIR - Adamsson, Annika
IR  - Ahonen S
FIR - Ahonen, Suvi
IR  - Hekkala MAA
FIR - Hekkala, Mari Akerlund Anne
IR  - Holappa H
FIR - Holappa, Henna
IR  - Hyoty H
FIR - Hyoty, Heikki
IR  - Ikonen A
FIR - Ikonen, Anni
IR  - Ilonen J
FIR - Ilonen, Jorma
IR  - Jaminki S
FIR - Jaminki, Sinikka
IR  - Jokipuu S
FIR - Jokipuu, Sanna
IR  - Karlsson L
FIR - Karlsson, Leena
IR  - Kahonen M
FIR - Kahonen, Miia
IR  - Knip M
FIR - Knip, Mikael
IR  - Koivikko ML
FIR - Koivikko, Minna-Liisa
IR  - Koreasalo M
FIR - Koreasalo, Mirva
IR  - Kurppa K
FIR - Kurppa, Kalle
IR  - Kytola J
FIR - Kytola, Jarita
IR  - Latva-Aho T
FIR - Latva-Aho, Tiina
IR  - Lindfors K
FIR - Lindfors, Katri
IR  - Lonnrot M
FIR - Lonnrot, Maria
IR  - Mantymaki E
FIR - Mantymaki, Elina
IR  - Mattila M
FIR - Mattila, Markus
IR  - Multasuo K
FIR - Multasuo, Katja
IR  - Mykkanen T
FIR - Mykkanen, Teija
IR  - Niininen T
FIR - Niininen, Tiina
IR  - Niinisto S
FIR - Niinisto, Sari
IR  - Nyblom M
FIR - Nyblom, Mia
IR  - Oikarinen S
FIR - Oikarinen, Sami
IR  - Ollikainen P
FIR - Ollikainen, Paula
IR  - Pohjola S
FIR - Pohjola, Sirpa
IR  - Rajala P
FIR - Rajala, Petra
IR  - Rautanen J
FIR - Rautanen, Jenna
IR  - Riikonen A
FIR - Riikonen, Anne
IR  - Romo M
FIR - Romo, Minna
IR  - Ruohonen S
FIR - Ruohonen, Suvi
IR  - Simell S
FIR - Simell, Satu
IR  - Sjoberg M
FIR - Sjoberg, Maija
IR  - Stenius A
FIR - Stenius, Aino
IR  - Tossavainen P
FIR - Tossavainen, Paivi
IR  - Vaha-Makila M
FIR - Vaha-Makila, Mari
IR  - Vainionpaa S
FIR - Vainionpaa, Sini
IR  - Varjonen E
FIR - Varjonen, Eeva
IR  - Veijola R
FIR - Veijola, Riitta
IR  - Viinikangas I
FIR - Viinikangas, Irene
IR  - Virtanen SM
FIR - Virtanen, Suvi M
IR  - She JX
FIR - She, Jin-Xiong
IR  - Schatz D
FIR - Schatz, Desmond
IR  - Hopkins D
FIR - Hopkins, Diane
IR  - Steed L
FIR - Steed, Leigh
IR  - Bryant J
FIR - Bryant, Jennifer
IR  - Silvis K
FIR - Silvis, Katherine
IR  - Haller M
FIR - Haller, Michael
IR  - Gardiner M
FIR - Gardiner, Melissa
IR  - McIndoe R
FIR - McIndoe, Richard
IR  - Sharma A
FIR - Sharma, Ashok
IR  - Anderson SW
FIR - Anderson, Stephen W
IR  - Jacobsen L
FIR - Jacobsen, Laura
IR  - Marks J
FIR - Marks, John
IR  - Towe PD
FIR - Towe, P D
IR  - Ziegler AG
FIR - Ziegler, Anette G
IR  - Bonifacio E
FIR - Bonifacio, Ezio
IR  - D'Angelo M
FIR - D'Angelo, Miryam
IR  - Gavrisan A
FIR - Gavrisan, Anita
IR  - Gezginci C
FIR - Gezginci, Cigdem
IR  - Heublein A
FIR - Heublein, Anja
IR  - Hoffmann V
FIR - Hoffmann, Verena
IR  - Hummel S
FIR - Hummel, Sandra
IR  - Keimer A
FIR - Keimer, Andrea
IR  - Knopff A
FIR - Knopff, Annette
IR  - Koch C
FIR - Koch, Charlotte
IR  - Koletzko S
FIR - Koletzko, Sibylle
IR  - Ramminger C
FIR - Ramminger, Claudia
IR  - Roth R
FIR - Roth, Roswith
IR  - Scholz M
FIR - Scholz, Marlon
IR  - Stock J
FIR - Stock, Joanna
IR  - Warncke K
FIR - Warncke, Katharina
IR  - Wendel L
FIR - Wendel, Lorena
IR  - Winkler C
FIR - Winkler, Christiane
IR  - Lernmark A
FIR - Lernmark, Ake
IR  - Agardh D
FIR - Agardh, Daniel
IR  - Aronsson CA
FIR - Aronsson, Carin Andren
IR  - Ask M
FIR - Ask, Maria
IR  - Bremer J
FIR - Bremer, Jenny
IR  - Cilio C
FIR - Cilio, Corrado
IR  - Ericson-Hallstrom E
FIR - Ericson-Hallstrom, Emelie
IR  - Fors A
FIR - Fors, Annika
IR  - Fransson L
FIR - Fransson, Lina
IR  - Gard T
FIR - Gard, Thomas
IR  - Bennet R
FIR - Bennet, Rasmus
IR  - Hansen M
FIR - Hansen, Monika
IR  - Hyberg S
FIR - Hyberg, Susanne
IR  - Jisser H
FIR - Jisser, Hanna
IR  - Johansen F
FIR - Johansen, Fredrik
IR  - Jonsdottir B
FIR - Jonsdottir, Berglind
IR  - Jovic S
FIR - Jovic, Silvija
IR  - Larsson HE
FIR - Larsson, Helena Elding
IR  - Lindstrom M
FIR - Lindstrom, Marielle
IR  - Lundgren M
FIR - Lundgren, Markus
IR  - Mansson-Martinez M
FIR - Mansson-Martinez, Maria
IR  - Markan M
FIR - Markan, Maria
IR  - Melin J
FIR - Melin, Jessica
IR  - Mestan Z
FIR - Mestan, Zeliha
IR  - Nilsson C
FIR - Nilsson, Caroline
IR  - Ottosson K
FIR - Ottosson, Karin
IR  - Rahmati K
FIR - Rahmati, Kobra
IR  - Ramelius A
FIR - Ramelius, Anita
IR  - Salami F
FIR - Salami, Falastin
IR  - Sjoberg A
FIR - Sjoberg, Anette
IR  - Sjoberg B
FIR - Sjoberg, Birgitta
IR  - Torn C
FIR - Torn, Carina
IR  - Wallin A
FIR - Wallin, Anne
IR  - Wimar A
FIR - Wimar, Asa
IR  - Aberg S
FIR - Aberg, Sofie
IR  - Hagopian WA
FIR - Hagopian, William A
IR  - Killian M
FIR - Killian, Michael
IR  - Crouch CC
FIR - Crouch, Claire Cowen
IR  - Skidmore J
FIR - Skidmore, Jennifer
IR  - Akramoff A
FIR - Akramoff, Ashley
IR  - Chavoshi M
FIR - Chavoshi, Masumeh
IR  - Dunson K
FIR - Dunson, Kayleen
IR  - Hervey R
FIR - Hervey, Rachel
IR  - Lyons R
FIR - Lyons, Rachel
IR  - Meyer A
FIR - Meyer, Arlene
IR  - Mulenga D
FIR - Mulenga, Denise
IR  - Radtke J
FIR - Radtke, Jared
IR  - Romancik M
FIR - Romancik, Matei
IR  - Schmitt D
FIR - Schmitt, Davey
IR  - Schwabe J
FIR - Schwabe, Julie
IR  - Zink S
FIR - Zink, Sarah
IR  - Becker D
FIR - Becker, Dorothy
IR  - Franciscus M
FIR - Franciscus, Margaret
IR  - Smith MD
FIR - Smith, MaryEllen Dalmagro-Elias
IR  - Daftary A
FIR - Daftary, Ashi
IR  - Klein MB
FIR - Klein, Mary Beth
IR  - Yates C
FIR - Yates, Chrystal
IR  - Krischer JP
FIR - Krischer, Jeffrey P
IR  - Austin-Gonzalez S
FIR - Austin-Gonzalez, Sarah
IR  - Avendano M
FIR - Avendano, Maryouri
IR  - Baethke S
FIR - Baethke, Sandra
IR  - Brown R
FIR - Brown, Rasheedah
IR  - Burkhardt B
FIR - Burkhardt, Brant
IR  - Butterworth M
FIR - Butterworth, Martha
IR  - Clasen J
FIR - Clasen, Joanna
IR  - Cuthbertson D
FIR - Cuthbertson, David
IR  - Eberhard C
FIR - Eberhard, Christopher
IR  - Fiske S
FIR - Fiske, Steven
IR  - Garmeson J
FIR - Garmeson, Jennifer
IR  - Gowda V
FIR - Gowda, Veena
IR  - Heyman K
FIR - Heyman, Kathleen
IR  - Hsiao B
FIR - Hsiao, Belinda
IR  - Karges C
FIR - Karges, Christina
IR  - Laras FP
FIR - Laras, Francisco Perez
IR  - Lee HS
FIR - Lee, Hye-Seung
IR  - Li Q
FIR - Li, Qian
IR  - Liu S
FIR - Liu, Shu
IR  - Liu X
FIR - Liu, Xiang
IR  - Lynch K
FIR - Lynch, Kristian
IR  - Maguire C
FIR - Maguire, Colleen
IR  - Malloy J
FIR - Malloy, Jamie
IR  - McCarthy C
FIR - McCarthy, Cristina
IR  - Merrell A
FIR - Merrell, Aubrie
IR  - Meulemans S
FIR - Meulemans, Steven
IR  - Parikh H
FIR - Parikh, Hemang
IR  - Quigley R
FIR - Quigley, Ryan
IR  - Remedios C
FIR - Remedios, Cassandra
IR  - Shaffer C
FIR - Shaffer, Chris
IR  - Smith L
FIR - Smith, Laura
IR  - Smith S
FIR - Smith, Susan
IR  - Sulman N
FIR - Sulman, Noah
IR  - Tamura R
FIR - Tamura, Roy
IR  - Tewey D
FIR - Tewey, Dena
IR  - Toth M
FIR - Toth, Michael
IR  - Uusitalo U
FIR - Uusitalo, Ulla
IR  - Vehik K
FIR - Vehik, Kendra
IR  - Vijayakandipan P
FIR - Vijayakandipan, Ponni
IR  - Wood K
FIR - Wood, Keith
IR  - Yang J
FIR - Yang, Jimin
IR  - Yu L
FIR - Yu, Liping
IR  - Miao D
FIR - Miao, Dongmei
IR  - Bingley P
FIR - Bingley, Polly
IR  - Williams A
FIR - Williams, Alistair
IR  - Chandler K
FIR - Chandler, Kyla
IR  - Ball O
FIR - Ball, Olivia
IR  - Kelland I
FIR - Kelland, Ilana
IR  - Grace S
FIR - Grace, Sian
IR  - Gillard B
FIR - Gillard, Ben
IR  - Hagopian W
FIR - Hagopian, William
IR  - Chavoshi M
FIR - Chavoshi, Masumeh
IR  - Radtke J
FIR - Radtke, Jared
IR  - Schwabe J
FIR - Schwabe, Julie
IR  - Erlich H
FIR - Erlich, Henry
IR  - Mack SJ
FIR - Mack, Steven J
IR  - Fear AL
FIR - Fear, Anna Lisa
IR  - Ke S
FIR - Ke, Sandra
IR  - Mulholland N
FIR - Mulholland, Niveen
IR  - Rich SS
FIR - Rich, Stephen S
IR  - Chen WM
FIR - Chen, Wei-Min
IR  - Onengut-Gumuscu S
FIR - Onengut-Gumuscu, Suna
IR  - Farber E
FIR - Farber, Emily
IR  - Pickin RR
FIR - Pickin, Rebecca Roche
IR  - Davis J
FIR - Davis, Jonathan
IR  - Davis J
FIR - Davis, Jordan
IR  - Gallo D
FIR - Gallo, Dan
IR  - Bonnie J
FIR - Bonnie, Jessica
IR  - Campolieto P
FIR - Campolieto, Paul
IR  - Akolkar B
FIR - Akolkar, Beena
IR  - Bourcier K
FIR - Bourcier, Kasia
IR  - Briese T
FIR - Briese, Thomas
IR  - Johnson SB
FIR - Johnson, Suzanne Bennett
IR  - Triplett E
FIR - Triplett, Eric
EDAT- 2019/04/11 06:00
MHDA- 2019/04/11 06:00
CRDT- 2019/04/11 06:00
PHST- 2018/11/01 00:00 [received]
PHST- 2019/03/12 00:00 [accepted]
PHST- 2019/04/11 06:00 [entrez]
PHST- 2019/04/11 06:00 [pubmed]
PHST- 2019/04/11 06:00 [medline]
AID - dc18-2282 [pii]
AID - 10.2337/dc18-2282 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Apr 9. pii: dc18-2282. doi: 10.2337/dc18-2282.

PMID- 30977833
OWN - NLM
STAT- Publisher
LR  - 20190412
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Apr 12
TI  - Endothelial function, adipokine serum levels and white matter hyperintesities in 
      subjects with diabetic foot syndrome.
LID - jc.2018-02507 [pii]
LID - 10.1210/jc.2018-02507 [doi]
AB  - CONTEXT: No study analysed the prevalence of white matter hyperintesities (WMHs) 
      in subjects with diabetic foot syndrome (DFS) and their relationship with
      adipokine serum levels and indexes of endothelial and cognitive performance.
      OBJECTIVE: To evaluate omentin and vaspin serum levels and WMHs prevalence in
      subjects with DFS and to analyse their relationship with other endothelial,
      arterial stiffness and cognitive function. RESEARCH DESIGN AND METHODS:
      Case-control study enrolling 40 subjects with DFS, 40 diabetic subjects without
      foot complications, 40 controls with foot lesions without diabetes and 40
      patients without diabetes mellitus. MAIN OUTCOME MEASURE: Pulse wave velocity
      (PWV), augmentation index (Aix), Reactive hyperemia index (RHI), serum vaspin and
      omentin levels, Fazekas Score, MMSE. RESULTS: Subjects with DFS showed higher
      mean PWV values if compared with diabetic controls, lower RHI values if compared 
      with controls. They also showed a lower mean MMSE score, significantly lower
      omentin serum levels, a higher prevalence of grade 2 severity of periventricular 
      hyperintensities (PVH). We observed a significant positive correlation between
      PWV and PVH, between Fazekas Score and PWV among diabetic subjects, whereas among
      subjects with diabetic foot we observed a significant negative correlation
      between PVH and RHI. CONCLUSIONS: Diabetes seems to be more associated with
      endothelial function disturbance in comparison with patients with diabetic foot
      that exhibit a more strict association with microvascular brain damage as
      indicated by our significant finding of an association with periventricular
      hyperintensities.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Tuttolomondo, Antonino
AU  - Tuttolomondo A
FAU - Di Raimondo, Domenico
AU  - Di Raimondo D
FAU - Casuccio, Alessandra
AU  - Casuccio A
AD  - Department of Promoting Health, Maternal-Infant. Excellence and Internal and
      Specialized Medicine G. D'Alessandro, University of Palermo ( Italy).
FAU - Guercio, Giovanni
AU  - Guercio G
AD  - Department of Surgical, Oncological and Oral Sciences (Di.Chir.On.S.).
FAU - Del Cuore, Alessandro
AU  - Del Cuore A
FAU - Puleo, Maria Grazia
AU  - Puleo MG
AD  - Internal Medicine and Stroke Care Ward, Department of Promoting Health,
      Maternal-Infant. Excellence and Internal and Specialized Medicine G.
      D'Alessandro, University of Palermo ( Italy).
FAU - Della Corte, Vittoriano
AU  - Della Corte V
AD  - Internal Medicine and Stroke Care Ward, Department of Promoting Health,
      Maternal-Infant. Excellence and Internal and Specialized Medicine G.
      D'Alessandro, University of Palermo ( Italy).
FAU - Bellia, Chiara
AU  - Bellia C
AD  - Section of Clinical Biochemistry and Molecular Biology, Department of
      Biopathology and Medical Biotechnologies (Di.Bi.Med.), University of Palermo.
FAU - Caronia, Aurelio
AU  - Caronia A
AD  - Triolo Zancla Home Care, Palermo.
FAU - Maida, Carlo
AU  - Maida C
AD  - Internal Medicine and Stroke Care Ward, Department of Promoting Health,
      Maternal-Infant. Excellence and Internal and Specialized Medicine G.
      D'Alessandro, University of Palermo ( Italy).
FAU - Pecoraro, Rosaria
AU  - Pecoraro R
AD  - Internal Medicine and Stroke Care Ward, Department of Promoting Health,
      Maternal-Infant. Excellence and Internal and Specialized Medicine G.
      D'Alessandro, University of Palermo ( Italy).
FAU - Simonetta, Irene
AU  - Simonetta I
AD  - Internal Medicine and Stroke Care Ward, Department of Promoting Health,
      Maternal-Infant. Excellence and Internal and Specialized Medicine G.
      D'Alessandro, University of Palermo ( Italy).
FAU - Gulotta, Gaspare
AU  - Gulotta G
AD  - Department of Surgical, Oncological and Oral Sciences (Di.Chir.On.S.).
FAU - Ciaccio, Marcello
AU  - Ciaccio M
AD  - Section of Clinical Biochemistry and Molecular Biology, Department of
      Biopathology and Medical Biotechnologies (Di.Bi.Med.), University of Palermo.
FAU - Pinto, Antonio
AU  - Pinto A
AD  - Internal Medicine and Stroke Care Ward, Department of Promoting Health,
      Maternal-Infant. Excellence and Internal and Specialized Medicine G.
      D'Alessandro, University of Palermo ( Italy).
LA  - eng
PT  - Journal Article
DEP - 20190412
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/04/13 06:00
MHDA- 2019/04/13 06:00
CRDT- 2019/04/13 06:00
PHST- 2018/11/20 00:00 [received]
PHST- 2019/04/08 00:00 [accepted]
PHST- 2019/04/13 06:00 [entrez]
PHST- 2019/04/13 06:00 [pubmed]
PHST- 2019/04/13 06:00 [medline]
AID - 5445421 [pii]
AID - 10.1210/jc.2018-02507 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Apr 12. pii: 5445421. doi: 10.1210/jc.2018-02507.

PMID- 30977832
OWN - NLM
STAT- Publisher
LR  - 20190412
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Apr 12
TI  - Identifying Pathogenic Variants of Monogenic Diabetes Using Targeted Panel
      Sequencing in an East Asian Population.
LID - jc.2018-02397 [pii]
LID - 10.1210/jc.2018-02397 [doi]
AB  - PURPOSE: Monogenic diabetes is a specific type of diabetes in which precision
      medicine could be applied. In this study, we used targeted panel sequencing to
      investigate pathogenic variants in Korean patients clinically suspected to have
      monogenic diabetes. METHODS: The eligibility criteria for inclusion were non-type
      1 diabetes patients with an age of onset </= 30 years and a BMI (body mass index)
      </= 30 kg/m2. Among the 2,090 non-type 1 diabetes patients, 109 were suspected to
      have monogenic diabetes and subjected to genetic testing. We analyzed 30
      monogenic diabetes genes using targeted panel sequencing. The pathogenicity of
      the genetic variants was evaluated according to the American College of Medical
      Genetics and Genomics and the Association for Molecular Pathology guidelines.
      RESULTS: Among the 109 suspected monogenic diabetes patients, 23 (21.1%) patients
      harbored pathogenic/likely pathogenic variants. A total of 14 pathogenic/likely
      pathogenic variants of common maturity onset diabetes of the young (MODY) genes
      were identified in GCK, HNF1A, HNF4A, and HNF1B. Other pathogenic/likely
      pathogenic variants were identified in WFS1, INS, ABCC8 and FOXP3. The
      mitochondrial DNA 3243 A>G variant was identified in five participants. Patients 
      with pathogenic/likely pathogenic variants had a significantly higher MODY
      probability, a lower BMI, and a lower C-peptide level than those without
      pathogenic/likely pathogenic variants (P=0.007, P=0.001, and P=0.012,
      respectively). CONCLUSIONS: Using targeted panel sequencing followed by
      pathogenicity evaluation, we were able to make molecular genetic diagnoses for 23
      (21.1%) suspected monogenic diabetes patients. Lower BMI, higher MODY
      probability, and lower C-peptide levels were characteristics of these
      participants.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Park, Seung Shin
AU  - Park SS
AD  - Department of Internal Medicine, Seoul National University Hospital, Seoul,
      Republic of Korea.
FAU - Jang, Se Song
AU  - Jang SS
AD  - Department of Biomedical Sciences, Seoul National University Graduate School,
      Seoul, Republic of Korea.
FAU - Ahn, Chang Ho
AU  - Ahn CH
AD  - Department of Internal Medicine, Seoul National University Hospital, Seoul,
      Republic of Korea.
FAU - Kim, Jung Hee
AU  - Kim JH
AD  - Department of Internal Medicine, Seoul National University Hospital, Seoul,
      Republic of Korea.
FAU - Jung, Hye Seung
AU  - Jung HS
AD  - Department of Internal Medicine, Seoul National University Hospital, Seoul,
      Republic of Korea.
FAU - Cho, Young Min
AU  - Cho YM
AD  - Department of Internal Medicine, Seoul National University Hospital, Seoul,
      Republic of Korea.
AD  - Department of Internal Medicine, Seoul National University College of Medicine,
      Seoul, Republic of Korea.
FAU - Lee, Young Ah
AU  - Lee YA
AD  - Department of Pediatrics, Seoul National University Hospital, Seoul, Republic of 
      Korea.
FAU - Shin, Choong Ho
AU  - Shin CH
AD  - Department of Pediatrics, Seoul National University Hospital, Seoul, Republic of 
      Korea.
AD  - Department of Pediatrics, Seoul National University College of Medicine, Seoul,
      Republic of Korea.
FAU - Chae, Jong Hee
AU  - Chae JH
AD  - Department of Pediatrics, Seoul National University Hospital, Seoul, Republic of 
      Korea.
AD  - Department of Pediatrics, Seoul National University College of Medicine, Seoul,
      Republic of Korea.
FAU - Kim, Jae Hyun
AU  - Kim JH
AD  - Department of Pediatrics, Seoul National University Bundang Hospital, Seongnam,
      Republic of Korea.
FAU - Choi, Sung Hee
AU  - Choi SH
AD  - Department of Internal Medicine, Seoul National University College of Medicine,
      Seoul, Republic of Korea.
AD  - Department of Internal Medicine, Seoul National University Bundang Hospital.
FAU - Jang, Hak C
AU  - Jang HC
AD  - Department of Internal Medicine, Seoul National University College of Medicine,
      Seoul, Republic of Korea.
AD  - Department of Internal Medicine, Seoul National University Bundang Hospital.
FAU - Bae, Jee Cheol
AU  - Bae JC
AD  - Department of Internal Medicine, Samsung Changwon Hospital, Changwon, Republic of
      Korea.
FAU - Won, Jong Cheol
AU  - Won JC
AD  - Department of Internal Medicine, Sanggye Paik Hospital, Seoul, Republic of Korea.
FAU - Kim, Sung-Hoon
AU  - Kim SH
AD  - Department of Internal Medicine, Cheil General Hospital & Women's Healthcare
      Center, Seoul, Republic of Korea.
AD  - Department of Internal Medicine, Dankook University College of Medicine, Seoul,
      Republic of Korea.
FAU - Kim, Jong-Il
AU  - Kim JI
AD  - Department of Biomedical Sciences, Seoul National University Graduate School,
      Seoul, Republic of Korea.
AD  - Department of Biochemistry and Molecular Biology, Seoul National University
      College of Medicine, Seoul, Republic of Korea.
AD  - Genomic Medicine Institute, Medical Research Center, Seoul National University,
      Seoul, Republic of Korea.
FAU - Kwak, Soo Heon
AU  - Kwak SH
AD  - Department of Internal Medicine, Seoul National University Hospital, Seoul,
      Republic of Korea.
FAU - Park, Kyong Soo
AU  - Park KS
AD  - Department of Internal Medicine, Seoul National University Hospital, Seoul,
      Republic of Korea.
AD  - Department of Internal Medicine, Seoul National University College of Medicine,
      Seoul, Republic of Korea.
AD  - Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School 
      of Convergence Science and Technology, Seoul National University, Seoul, Republic
      of Korea.
LA  - eng
PT  - Journal Article
DEP - 20190412
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/04/13 06:00
MHDA- 2019/04/13 06:00
CRDT- 2019/04/13 06:00
PHST- 2018/11/06 00:00 [received]
PHST- 2019/04/08 00:00 [accepted]
PHST- 2019/04/13 06:00 [entrez]
PHST- 2019/04/13 06:00 [pubmed]
PHST- 2019/04/13 06:00 [medline]
AID - 5445415 [pii]
AID - 10.1210/jc.2018-02397 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Apr 12. pii: 5445415. doi: 10.1210/jc.2018-02397.

PMID- 30958544
OWN - NLM
STAT- Publisher
LR  - 20190408
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Apr 8
TI  - Effect of the GLP-1 receptor agonist exenatide on impaired awareness of
      hypoglycemia in type 1 diabetes; a randomized controlled trial.
LID - jc.2019-00087 [pii]
LID - 10.1210/jc.2019-00087 [doi]
AB  - CONTEXT: Impaired awareness of hypoglycemia (IAH), resulting from habituation to 
      recurrent hypoglycemia, can be reversed by strict avoidance of hypoglycemia.
      Adjunctive treatment with glucagon-like peptide-1 (GLP-1) receptor agonists may
      reduce glucose variability, hence lower the risk of hypoglycemia and improve
      awareness. The aim of our study was to investigate the effect of exenatide on
      awareness of hypoglycemia in people with type 1 diabetes and IAH. METHODS: This
      was a randomized double-blind, placebo-controlled cross-over trial. Ten patients 
      with type 1 diabetes and IAH were included (age 38.5+/-4.4 years, 40% males,
      HbA1c 7.2+/-0.4 % (55.2+/-4.8 mmol/mol)). Patients were treated with exenatide
      5microg twice daily (first 2 weeks), followed by 10microg twice daily (remaining 
      4 weeks) or matching placebo, with a 4-week washout period. Patients wore blinded
      glucose sensors in the final weeks and modified hyperinsulinemic
      normoglycemic-hypoglycemic glucose clamps (nadir 2.5 mmol/l) were performed at
      the end of each treatment period. RESULTS: Treatment with exenatide caused body
      weight to fall as compared to placebo (-3.9+/-0.9 vs. 0.6+/-1.2 kg, p=0.047).
      Exenatide did not change mean 24-hour glucose levels (8.3+/-0.4 vs. 8.5+/-0.3
      mmol/l, exenatide vs. placebo, p=0.64), median (interquartile range) percentage
      of time spent in hypoglycemia (15.5 [4.5, 25.5] vs. 7.8 [4.4, 17.1]%, p=0.11) and
      frequency of hypoglycemia (15.8+/-3.7 vs. 12.1+/-3.5, p=0.19). Symptom scores in 
      response to clamped hypoglycemia were similar between exenatide (median change
      1.0 [-1.5, 7.0]) and placebo (4.5 [1.5, 5.8], p=0.08). CONCLUSIONS: Six weeks
      treatment with exenatide did not improve awareness of hypoglycemia in patients
      with type 1 diabetes and IAH.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - van Meijel, Lian A
AU  - van Meijel LA
AD  - Department of Internal Medicine, Radboud university medical center, Nijmegen, the
      Netherlands.
FAU - Rooijackers, Hanne M
AU  - Rooijackers HM
AD  - Department of Internal Medicine, Radboud university medical center, Nijmegen, the
      Netherlands.
FAU - Tack, Cees J
AU  - Tack CJ
AD  - Department of Internal Medicine, Radboud university medical center, Nijmegen, the
      Netherlands.
FAU - de Galan, Bastiaan E
AU  - de Galan BE
AD  - Department of Internal Medicine, Radboud university medical center, Nijmegen, the
      Netherlands.
LA  - eng
PT  - Journal Article
DEP - 20190408
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/04/09 06:00
MHDA- 2019/04/09 06:00
CRDT- 2019/04/09 06:00
PHST- 2019/01/11 00:00 [received]
PHST- 2019/04/02 00:00 [accepted]
PHST- 2019/04/09 06:00 [entrez]
PHST- 2019/04/09 06:00 [pubmed]
PHST- 2019/04/09 06:00 [medline]
AID - 5428134 [pii]
AID - 10.1210/jc.2019-00087 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Apr 8. pii: 5428134. doi: 10.1210/jc.2019-00087.