PMID- 30944112
OWN - NLM
STAT- MEDLINE
DCOM- 20190415
LR  - 20190418
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Linking)
VI  - 365
DP  - 2019 Apr 3
TI  - Continuous subcutaneous insulin infusion versus multiple daily injection regimens
      in children and young people at diagnosis of type 1 diabetes: pragmatic
      randomised controlled trial and economic evaluation.
PG  - l1226
LID - 10.1136/bmj.l1226 [doi]
AB  - OBJECTIVE: To compare the efficacy, safety, and cost utility of continuous
      subcutaneous insulin infusion (CSII) with multiple daily injection (MDI) regimens
      during the first year following diagnosis of type 1 diabetes in children and
      young people. DESIGN: Pragmatic, multicentre, open label, parallel group,
      randomised controlled trial and economic evaluation. SETTING: 15 paediatric
      National Health Service (NHS) diabetes services in England and Wales. The study
      opened to recruitment in May 2011 and closed in January 2017. PARTICIPANTS:
      Patients aged between 7 months and 15 years, with a new diagnosis of type 1
      diabetes were eligible to participate. Patients who had a sibling with the
      disease, and those who took drug treatments or had additional diagnoses that
      could have affected glycaemic control were ineligible. INTERVENTIONS:
      Participants were randomised, stratified by age and treating centre, to start
      treatment with CSII or MDI within 14 days of diagnosis. Starting doses of aspart 
      (CSII and MDI) and glargine or detemir (MDI) were calculated according to weight 
      and age, and titrated according to blood glucose measurements and according to
      local clinical practice. MAIN OUTCOME MEASURES: Primary outcome was glycaemic
      control (as measured by glycated haemoglobin; HbA1c) at 12 months. Secondary
      outcomes were percentage of patients in each treatment arm with HbA1c within the 
      national target range, incidence of severe hypoglycaemia and diabetic
      ketoacidosis, change in height and body mass index (as measured by standard
      deviation scores), insulin requirements (units/kg/day), partial remission rate
      (insulin dose adjusted HbA1c <9), paediatric quality of life inventory score, and
      cost utility based on the incremental cost per quality adjusted life year (QALY) 
      gained from an NHS costing perspective. RESULTS: 294 participants were randomised
      and 293 included in intention to treat analyses (CSI, n=144; MDI, n=149). At 12
      months, mean HbA1c was comparable with clinically unimportant differences between
      CSII and MDI participants (60.9 mmol/mol v 58.5 mmol/mol, mean difference 2.4
      mmol/mol (95% confidence interval -0.4 to 5.3), P=0.09). Achievement of HbA1c
      lower than 58 mmol/mol was low among the two groups (66/143 (46%) CSII
      participants v 78/142 (55%) MDI participants; relative risk 0.84 (95% confidence 
      interval 0.67 to 1.06)). Incidence of severe hypoglycaemia and diabetic
      ketoacidosis were low in both groups. Fifty four non-serious and 14 serious
      adverse events were reported during CSII treatment, and 17 non-serious and eight 
      serious adverse events during MDI treatment. Parents (but not children) reported 
      superior PedsQL scores for those patients treated with CSII compared to those
      treated with MDI. CSII was more expensive than MDI by pound1863 (euro2179; $2474;
      95% confidence interval pound1620 to pound2137) per patient, with no additional
      QALY gains (difference -0.006 (95% confidence interval -0.031 to 0.018)).
      CONCLUSION: During the first year following type 1 diabetes diagnosis, no
      clinical benefit of CSII over MDI was identified in children and young people in 
      the UK setting, and treatment with either regimen was suboptimal in achieving
      HbA1c thresholds. CSII was not cost effective. TRIAL REGISTRATION: Current
      Controlled Trials ISRCTN29255275; European Clinical Trials Database
      2010-023792-25.
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 - Blair, Joanne C
AU  - Blair JC
AUID- ORCID: 0000-0003-3128-5574
AD  - Department of Endocrinology, Alder Hey Children's NHS Foundation Trust, Liverpool
      L12 2AP, UK jo.blair@alderhey.nhs.uk.
FAU - McKay, Andrew
AU  - McKay A
AD  - Clinical Trials Research Centre, University of Liverpool, Liverpool, UK.
FAU - Ridyard, Colin
AU  - Ridyard C
AD  - Centre for Health Economics and Medicines Evaluation, Bangor University, Bangor, 
      UK.
FAU - Thornborough, Keith
AU  - Thornborough K
AD  - Department of Diabetes, Alder Hey Children's NHS Foundation Trust, Liverpool, UK.
FAU - Bedson, Emma
AU  - Bedson E
AD  - Clinical Trials Research Centre, University of Liverpool, Liverpool, UK.
FAU - Peak, Matthew
AU  - Peak M
AD  - Department of Research, Alder Hey Children's NHS Foundation Trust, Liverpool, UK.
FAU - Didi, Mohammed
AU  - Didi M
AD  - Department of Endocrinology, Alder Hey Children's NHS Foundation Trust, Liverpool
      L12 2AP, UK.
FAU - Annan, Francesca
AU  - Annan F
AD  - Department of Diabetes, Alder Hey Children's NHS Foundation Trust, Liverpool, UK.
FAU - Gregory, John W
AU  - Gregory JW
AD  - Division of Population Medicine, School of Medicine, Cardiff University, Cardiff,
      UK.
FAU - Hughes, Dyfrig A
AU  - Hughes DA
AD  - Centre for Health Economics and Medicines Evaluation, Bangor University, Bangor, 
      UK.
FAU - Gamble, Carrol
AU  - Gamble C
AD  - Clinical Trials Research Centre, University of Liverpool, Liverpool, UK.
CN  - SCIPI investigators
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Multicenter Study
PT  - Pragmatic Clinical Trial
PT  - Research Support, Non-U.S. Gov't
DEP - 20190403
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
SB  - AIM
SB  - IM
MH  - Adolescent
MH  - Child
MH  - Child, Preschool
MH  - Cost-Benefit Analysis
MH  - Diabetes Mellitus, Type 1/*drug therapy/economics
MH  - Humans
MH  - Hypoglycemic Agents/*administration & dosage/adverse effects/economics
MH  - Infant
MH  - Injections, Subcutaneous
MH  - Insulin/*administration & dosage/adverse effects/economics
MH  - Insulin Infusion Systems
MH  - Quality of Life
MH  - Quality-Adjusted Life Years
MH  - Treatment Outcome
PMC - PMC6446076
COIS- Competing interests: All authors have completed the ICMJE uniform disclosure form
      at www.icmje.org/coi_disclosure.pdf and declare: support from the UK NIHR Health 
      Technology Assessment Programme for the submitted work; JCB undertakes paid
      advisory work, and has received funding for research, to attend academic meetings
      and to support a nursing salary from Novo Nordisk, a pharmaceutical company that 
      manufactures some of the insulins used in the SCIPI study (work for this company 
      relates to growth hormone therapy and not diabetes); MD has received payment for 
      advisory work, funding to attend academic meetings and to support a nursing
      salary from Novo Nordisk, a pharmaceutical company that manufactures some of the 
      insulins used in the SCIPI study (work for this company relates to growth hormone
      therapy and not diabetes), and has received expenses from Merk Serono to attend
      educational meetings; JWG is chairman of the NovoNordisk UK Foundation, receives 
      funding from NovoNordisk, Ipsen, Serono, and Pfizer to part support attendance at
      annual scientific meetings of the European Society for Paediatric Endocrinology, 
      and receives speaker's fees to talk on communication skills from Pfizer and
      Lilly; no other relationships or activities that could appear to have influenced 
      the submitted work.
EDAT- 2019/04/05 06:00
MHDA- 2019/04/16 06:00
CRDT- 2019/04/05 06:00
PHST- 2019/04/05 06:00 [entrez]
PHST- 2019/04/05 06:00 [pubmed]
PHST- 2019/04/16 06:00 [medline]
AID - 10.1136/bmj.l1226 [doi]
PST - epublish
SO  - BMJ. 2019 Apr 3;365:l1226. doi: 10.1136/bmj.l1226.

PMID- 30728129
OWN - NLM
STAT- MEDLINE
DCOM- 20190403
LR  - 20190403
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Linking)
VI  - 364
DP  - 2019 Feb 6
TI  - #TalkAboutComplications.
PG  - k5258
LID - 10.1136/bmj.k5258 [doi]
FAU - Scibilia, Renza
AU  - Scibilia R
FAU - Aldred, Chris
AU  - Aldred C
LA  - eng
PT  - Journal Article
DEP - 20190206
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
SB  - AIM
SB  - IM
MH  - *Communication
MH  - Diabetes Complications/*prevention & control/psychology
MH  - Humans
MH  - Professional-Patient Relations
MH  - *Risk Reduction Behavior
MH  - Semantics
MH  - Shame
COIS- Competing interests The BMJ has judged that there are no disqualifying financial 
      ties to commercial companies. The authors declare the following other interests: 
      Both authors have received funding from diabetes device and drug companies to
      attend events. Renza Scibilia was involved in the development of the Diabetes
      Australia Language Position Statement. Further details of The BMJ policy on
      financial interests is here:
      https://www.bmj.com/about-bmj/resources-authors/forms-policies-and-checklists/dec
      laration-competing-interests Provenance and peer review: Commissioned, based on
      an idea from the author; not externally peer reviewed.
EDAT- 2019/02/08 06:00
MHDA- 2019/04/04 06:00
CRDT- 2019/02/08 06:00
PHST- 2019/02/08 06:00 [entrez]
PHST- 2019/02/08 06:00 [pubmed]
PHST- 2019/04/04 06:00 [medline]
AID - 10.1136/bmj.k5258 [doi]
PST - epublish
SO  - BMJ. 2019 Feb 6;364:k5258. doi: 10.1136/bmj.k5258.

PMID- 30651232
OWN - NLM
STAT- MEDLINE
DCOM- 20190403
LR  - 20190403
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Linking)
VI  - 364
DP  - 2019 Jan 16
TI  - Common conditions associated with hereditary haemochromatosis genetic variants:
      cohort study in UK Biobank.
PG  - k5222
LID - 10.1136/bmj.k5222 [doi]
AB  - OBJECTIVE: To compare prevalent and incident morbidity and mortality between
      those with the HFE p.C282Y genetic variant (responsible for most hereditary
      haemochromatosis type 1) and those with no p.C282Y mutations, in a large UK
      community sample of European descent. DESIGN: Cohort study. SETTING: 22 centres
      across England, Scotland, and Wales in UK Biobank (2006-10). PARTICIPANTS: 451
      243 volunteers of European descent aged 40 to 70 years, with a mean follow-up of 
      seven years (maximum 9.4 years) through hospital inpatient diagnoses and death
      certification. MAIN OUTCOME MEASURE: Odds ratios and Cox hazard ratios of disease
      rates between participants with and without the haemochromatosis mutations,
      adjusted for age, genotyping array type, and genetic principal components. The
      sexes were analysed separately as morbidity due to iron excess occurs later in
      women. RESULTS: Of 2890 participants homozygous for p.C282Y (0.6%, or 1 in 156), 
      haemochromatosis was diagnosed in 21.7% (95% confidence interval 19.5% to 24.1%, 
      281/1294) of men and 9.8% (8.4% to 11.2%, 156/1596) of women by end of follow-up.
      p.C282Y homozygous men aged 40 to 70 had a higher prevalence of diagnosed
      haemochromatosis (odds ratio 411.1, 95% confidence interval 299.0 to 565.3,
      P<0.001), liver disease (4.30, 2.97 to 6.18, P<0.001), rheumatoid arthritis
      (2.23, 1.51 to 3.31, P<0.001), osteoarthritis (2.01, 1.71 to 2.36, P<0.001), and 
      diabetes mellitus (1.53, 1.16 to 1.98, P=0.002), versus no p.C282Y mutations
      (n=175 539). During the seven year follow-up, 15.7% of homozygous men developed
      at least one incident associated condition versus 5.0% (P<0.001) with no p.C282Y 
      mutations (women 10.1% v 3.4%, P<0.001). Haemochromatosis diagnoses were more
      common in p.C282Y/p.H63D heterozygotes, but excess morbidity was modest.
      CONCLUSIONS: In a large community sample, HFE p.C282Y homozygosity was associated
      with substantial prevalent and incident clinically diagnosed morbidity in both
      men and women. As p.C282Y associated iron overload is preventable and treatable
      if intervention starts early, these findings justify re-examination of options
      for expanded early case ascertainment and screening.
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 - Pilling, Luke C
AU  - Pilling LC
AD  - Epidemiology and Public Health Group, University of Exeter Medical School, RD&E
      Wonford, Exeter EX2 5DW, UK.
FAU - Tamosauskaite, Jone
AU  - Tamosauskaite J
AD  - Epidemiology and Public Health Group, University of Exeter Medical School, RD&E
      Wonford, Exeter EX2 5DW, UK.
FAU - Jones, Garan
AU  - Jones G
AD  - Epidemiology and Public Health Group, University of Exeter Medical School, RD&E
      Wonford, Exeter EX2 5DW, UK.
FAU - Wood, Andrew R
AU  - Wood AR
AD  - Genetics of Complex Traits Group, University of Exeter Medical School, Exeter,
      UK.
FAU - Jones, Lindsay
AU  - Jones L
AD  - Epidemiology and Public Health Group, University of Exeter Medical School, RD&E
      Wonford, Exeter EX2 5DW, UK.
FAU - Kuo, Chai-Ling
AU  - Kuo CL
AD  - Biostatistics Center, CT Institute for Clinical & Translational Science,
      University of Connecticut Health Center, Farmington, CT, USA.
FAU - Kuchel, George A
AU  - Kuchel GA
AD  - Center on Aging, University of Connecticut Health Center, Farmington, CT, USA.
FAU - Ferrucci, Luigi
AU  - Ferrucci L
AD  - National Institute on Aging, Baltimore, MD, USA.
FAU - Melzer, David
AU  - Melzer D
AUID- ORCID: 0000-0002-0170-3838
AD  - Epidemiology and Public Health Group, University of Exeter Medical School, RD&E
      Wonford, Exeter EX2 5DW, UK D.Melzer@exeter.ac.uk.
AD  - Center on Aging, University of Connecticut Health Center, Farmington, CT, USA.
LA  - eng
GR  - MC_QA137853/Medical Research Council/United Kingdom
GR  - Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20190116
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
RN  - 0 (HFE protein, human)
RN  - 0 (Hemochromatosis Protein)
SB  - AIM
SB  - IM
MH  - Adult
MH  - Aged
MH  - Arthritis, Rheumatoid/*epidemiology
MH  - Comorbidity
MH  - Diabetes Mellitus/*epidemiology
MH  - Female
MH  - Follow-Up Studies
MH  - Hemochromatosis/*epidemiology/*genetics
MH  - Hemochromatosis Protein/*genetics
MH  - Heterozygote
MH  - Homozygote
MH  - Humans
MH  - Incidence
MH  - Liver Diseases/*epidemiology
MH  - Male
MH  - Middle Aged
MH  - Mutation
MH  - Osteoarthritis/*epidemiology
MH  - Prevalence
MH  - United Kingdom
PMC - PMC6334179
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- 2019/01/18 06:00
MHDA- 2019/04/04 06:00
CRDT- 2019/01/18 06:00
PHST- 2019/01/18 06:00 [entrez]
PHST- 2019/01/18 06:00 [pubmed]
PHST- 2019/04/04 06:00 [medline]
AID - 10.1136/bmj.k5222 [doi]
PST - epublish
SO  - BMJ. 2019 Jan 16;364:k5222. doi: 10.1136/bmj.k5222.

PMID- 30626583
OWN - NLM
STAT- MEDLINE
DCOM- 20190403
LR  - 20190403
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Linking)
VI  - 364
DP  - 2019 Jan 9
TI  - Helen Salisbury: When policy doesn't match evidence.
PG  - l54
LID - 10.1136/bmj.l54 [doi]
FAU - Salisbury, Helen
AU  - Salisbury H
AD  - Oxford.
LA  - eng
PT  - Journal Article
DEP - 20190109
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
SB  - AIM
SB  - IM
MH  - *Attitude of Health Personnel
MH  - Attitude to Health
MH  - Diabetes Mellitus, Type 2/*prevention & control
MH  - Evidence-Based Practice
MH  - Health Policy
MH  - Humans
MH  - *Prediabetic State/psychology/therapy
COIS- Competing interests: I am a GP partner, I teach medical students at Oxford
      University and St Anne's College, Oxford, and I answer readers' medical problems 
      for Take A Break magazine. I am also a member of the National Health Action Party
      and serve on its national executive committee.
EDAT- 2019/01/11 06:00
MHDA- 2019/04/04 06:00
CRDT- 2019/01/11 06:00
PHST- 2019/01/11 06:00 [entrez]
PHST- 2019/01/11 06:00 [pubmed]
PHST- 2019/04/04 06:00 [medline]
AID - 10.1136/bmj.l54 [doi]
PST - epublish
SO  - BMJ. 2019 Jan 9;364:l54. doi: 10.1136/bmj.l54.

PMID- 30936151
OWN - NLM
STAT- Publisher
LR  - 20190402
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2019 Apr 1
TI  - Erratum. Sodium-Glucose Cotransporter 2 Inhibition and Diabetic Kidney Disease.
      Diabetes 2019;68:248-257.
LID - db19er05a [pii]
LID - 10.2337/db19-er05a [doi]
FAU - Alicic, Radica Z
AU  - Alicic RZ
FAU - Neumiller, Joshua J
AU  - Neumiller JJ
FAU - Johnson, Emily J
AU  - Johnson EJ
FAU - Dieter, Brad
AU  - Dieter B
FAU - Tuttle, Katherine R
AU  - Tuttle KR
LA  - eng
PT  - Journal Article
PT  - Published Erratum
DEP - 20190401
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
EFR - Diabetes. 2019 Feb;68(2):248-257. PMID: 30665953
EDAT- 2019/04/03 06:00
MHDA- 2019/04/03 06:00
CRDT- 2019/04/03 06:00
PHST- 2019/04/03 06:00 [entrez]
PHST- 2019/04/03 06:00 [pubmed]
PHST- 2019/04/03 06:00 [medline]
AID - db19-er05a [pii]
AID - 10.2337/db19-er05a [doi]
PST - aheadofprint
SO  - Diabetes. 2019 Apr 1. pii: db19-er05a. doi: 10.2337/db19-er05a.

PMID- 30936146
OWN - NLM
STAT- Publisher
LR  - 20190402
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2019 Apr 1
TI  - T Cell-Specific PTPN2-Deficiency in NOD Mice Accelerates the Development of Type 
      1 Diabetes and Autoimmune Co-Morbidities.
LID - db181362 [pii]
LID - 10.2337/db18-1362 [doi]
AB  - Genome-wide association studies have identified PTPN2 as an important non-major
      histocompatibility complex gene for autoimmunity. Single nucleotide polymorphisms
      that reduce PTPN2 expression have been linked with the development of varied
      autoimmune disorders, including type 1 diabetes. The tyrosine-phosphatase PTPN2
      attenuates T cell receptor and cytokine signalling in T cells to maintain
      peripheral tolerance, but the extent to which PTPN2-deficiency in T cells might
      influence type 1 diabetes onset remains unclear. Non-Obese Diabetic (NOD) mice
      develop spontaneous autoimmune type 1 diabetes, similar to that seen in humans. T
      cell PTPN2-deficiency in NOD mice markedly accelerated the onset and increased
      the incidence of type 1 diabetes, as well as that of other disorders, including
      colitis and Sjogren's syndrome. Although PTPN2-deficiency in CD8(+) T cells alone
      was able to drive the destruction of pancreatic beta cells and onset of diabetes,
      T cell-specific PTPN2-deficiency was also accompanied by increased CD4(+)
      T-helper type 1 differentiation and T follicular helper cell polarisation and an 
      increased abundance of B cells in pancreatic islets as seen in human type 1
      diabetes. These findings causally link PTPN2-deficiency in T cells with the
      development of type 1 diabetes and associated autoimmune co-morbidities.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Wiede, Florian
AU  - Wiede F
AD  - Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria
      3800, Australia, Tony.Tiganis@monash.edu Florian.Wiede@petermac.org.
AD  - Department of Biochemistry and Molecular Biology, Monash University, Clayton,
      Victoria 3800.
AD  - Peter MacCallum Cancer Centre, Melbourne, Victoria, 3000, Australia.
FAU - Brodnicki, Tom
AU  - Brodnicki T
AD  - St. Vincent's Institute, Fitzroy, Victoria 3065, Australia.
AD  - Department of Medicine, St. Vincent's Hospital, The University of Melbourne,
      Fitzroy, Victoria 3065, Australia.
FAU - Goh, Pei Kee
AU  - Goh PK
AD  - Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria
      3800, Australia.
AD  - Department of Biochemistry and Molecular Biology, Monash University, Clayton,
      Victoria 3800.
AD  - Peter MacCallum Cancer Centre, Melbourne, Victoria, 3000, Australia.
FAU - Leong, Yew A
AU  - Leong YA
AD  - Department of Biochemistry and Molecular Biology, Monash University, Clayton,
      Victoria 3800.
FAU - Jones, Gareth W
AU  - Jones GW
AD  - Division of Infection & Immunity, School of Medicine, Cardiff University,
      Cardiff, Wales, UK.
AD  - Systems Immunity University Research Institute, Cardiff University, Cardiff,
      Wales, UK.
AD  - School of Cellular and Molecular Medicine, University of Bristol, Bristol, UK.
FAU - Yu, Di
AU  - Yu D
AD  - Department of Biochemistry and Molecular Biology, Monash University, Clayton,
      Victoria 3800.
FAU - Baxter, Alan G
AU  - Baxter AG
AD  - Comparative Genomics Centre, James Cook University, Townsville, QLD, Australia.
FAU - Jones, Simon A
AU  - Jones SA
AD  - Division of Infection & Immunity, School of Medicine, Cardiff University,
      Cardiff, Wales, UK.
AD  - Systems Immunity University Research Institute, Cardiff University, Cardiff,
      Wales, UK.
FAU - Kay, Tom
AU  - Kay T
AD  - St. Vincent's Institute, Fitzroy, Victoria 3065, Australia.
AD  - Department of Medicine, St. Vincent's Hospital, The University of Melbourne,
      Fitzroy, Victoria 3065, Australia.
FAU - Tiganis, Tony
AU  - Tiganis T
AD  - Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria
      3800, Australia, Tony.Tiganis@monash.edu Florian.Wiede@petermac.org.
AD  - Department of Biochemistry and Molecular Biology, Monash University, Clayton,
      Victoria 3800.
AD  - Peter MacCallum Cancer Centre, Melbourne, Victoria, 3000, Australia.
LA  - eng
PT  - Journal Article
DEP - 20190401
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
EDAT- 2019/04/03 06:00
MHDA- 2019/04/03 06:00
CRDT- 2019/04/03 06:00
PHST- 2019/01/01 00:00 [received]
PHST- 2019/03/17 00:00 [accepted]
PHST- 2019/04/03 06:00 [entrez]
PHST- 2019/04/03 06:00 [pubmed]
PHST- 2019/04/03 06:00 [medline]
AID - db18-1362 [pii]
AID - 10.2337/db18-1362 [doi]
PST - aheadofprint
SO  - Diabetes. 2019 Apr 1. pii: db18-1362. doi: 10.2337/db18-1362.

PMID- 30936144
OWN - NLM
STAT- Publisher
LR  - 20190402
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2019 Apr 1
TI  - Diabetes-Associated Myelopoiesis Drives Stem Cell Mobilopathy Through an
      OSM-p66Shc Signaling Pathway.
LID - db190080 [pii]
LID - 10.2337/db19-0080 [doi]
AB  - Diabetes impairs the mobilization of hematopoietic stem/progenitor cells (HSPCs) 
      from the bone marrow (BM), which can worsen the outcomes of HSPC transplantation 
      and of diabetic complications. In this study, we examined the oncostatin M (OSM) 
      - p66Shc pathway as a mechanistic link between HSPC mobilopathy and excessive
      myelopoiesis. We found that streptozotocin (STZ)-induced diabetes in mice skewed 
      hematopoiesis towards the myeloid lineage, via hematopoietic-intrinsic p66Shc.
      The overexpression of Osm resulting from myelopoiesis prevented HSPC mobilization
      after G-CSF. The intimate link between myelopoiesis and impaired HSPC
      mobilization after G-CSF was confirmed in human diabetes. Using
      cross-transplantation experiments, we found that deletion of p66Shc in the
      hematopoietic or non-hematopoietic system partially rescued defective HSPC
      mobilization in diabetes. Additionally, p66Shc mediated the diabetes-induced BM
      microvasculature remodeling. Ubiquitous or hematopoietic restricted Osm deletion 
      phenocopied p66Shc deletion in preventing diabetes-associated myelopoiesis and
      mobilopathy. Mechanistically, we discovered that OSM couples myelopoiesis to
      mobilopathy by inducing Cxcl12 in BM stromal cells via non-mitochondrial p66Shc. 
      Altogether, these data indicate that cell-autonomous activation of the OSM-p66Shc
      pathway leads to diabetes-associated myelopoiesis, whereas its transcellular
      hemato-stromal activation links myelopoiesis to mobilopathy. Targeting the
      OSM-p66Shc pathway is a novel strategy to disconnect mobilopathy from
      myelopoiesis and restore normal HSPC mobilization.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Albiero, Mattia
AU  - Albiero M
AD  - Veneto Institute of Molecular Medicine (VIMM), 35129 Padova, Italy.
AD  - Department of Medicine - DIMED, University of Padova, 35128 Padova, Italy.
FAU - Ciciliot, Stefano
AU  - Ciciliot S
AD  - Veneto Institute of Molecular Medicine (VIMM), 35129 Padova, Italy.
FAU - Tedesco, Serena
AU  - Tedesco S
AD  - Veneto Institute of Molecular Medicine (VIMM), 35129 Padova, Italy.
AD  - Department of Medicine - DIMED, University of Padova, 35128 Padova, Italy.
FAU - Menegazzo, Lisa
AU  - Menegazzo L
AD  - Veneto Institute of Molecular Medicine (VIMM), 35129 Padova, Italy.
FAU - D'Anna, Marianna
AU  - D'Anna M
AD  - Veneto Institute of Molecular Medicine (VIMM), 35129 Padova, Italy.
AD  - Department of Medicine - DIMED, University of Padova, 35128 Padova, Italy.
FAU - Scattolini, Valentina
AU  - Scattolini V
AD  - Veneto Institute of Molecular Medicine (VIMM), 35129 Padova, Italy.
AD  - Department of Medicine - DIMED, University of Padova, 35128 Padova, Italy.
FAU - Cappellari, Roberta
AU  - Cappellari R
AD  - Veneto Institute of Molecular Medicine (VIMM), 35129 Padova, Italy.
AD  - Department of Medicine - DIMED, University of Padova, 35128 Padova, Italy.
FAU - Zuccolotto, Gaia
AU  - Zuccolotto G
AD  - Department of Surgery, Oncology and Gastroenterology, University of Padova, 35129
      Padova, Italy.
AD  - Istituto Oncologico Veneto IOV-IRCCS, 35128 Padova, Italy.
FAU - Rosato, Antonio
AU  - Rosato A
AD  - Department of Surgery, Oncology and Gastroenterology, University of Padova, 35129
      Padova, Italy.
AD  - Istituto Oncologico Veneto IOV-IRCCS, 35128 Padova, Italy.
FAU - Cignarella, Andrea
AU  - Cignarella A
AD  - Department of Medicine - DIMED, University of Padova, 35128 Padova, Italy.
FAU - Giorgio, Marco
AU  - Giorgio M
AD  - European Institute of Oncology (IEO), 20139 Milan, Italy.
AD  - Department of Biomedical Sciences, 35131 Padova, Italy.
FAU - Avogaro, Angelo
AU  - Avogaro A
AD  - Department of Medicine - DIMED, University of Padova, 35128 Padova, Italy.
FAU - Fadini, Gian Paolo
AU  - Fadini GP
AD  - Veneto Institute of Molecular Medicine (VIMM), 35129 Padova, Italy
      gianpaolofadini@hotmail.com.
AD  - Department of Medicine - DIMED, University of Padova, 35128 Padova, Italy.
LA  - eng
PT  - Journal Article
DEP - 20190401
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
EDAT- 2019/04/03 06:00
MHDA- 2019/04/03 06:00
CRDT- 2019/04/03 06:00
PHST- 2019/01/24 00:00 [received]
PHST- 2019/03/15 00:00 [accepted]
PHST- 2019/04/03 06:00 [entrez]
PHST- 2019/04/03 06:00 [pubmed]
PHST- 2019/04/03 06:00 [medline]
AID - db19-0080 [pii]
AID - 10.2337/db19-0080 [doi]
PST - aheadofprint
SO  - Diabetes. 2019 Apr 1. pii: db19-0080. doi: 10.2337/db19-0080.

PMID- 30940642
OWN - NLM
STAT- Publisher
LR  - 20190403
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Apr 2
TI  - Heart Rate, Autonomic Function, and Future Changes in Glucose Metabolism in
      Individuals Without Diabetes: The Whitehall II Cohort Study.
LID - dc181838 [pii]
LID - 10.2337/dc18-1838 [doi]
AB  - OBJECTIVE: Autonomic nervous system dysfunction is associated with impaired
      glucose metabolism, but the temporality of this association remains unclear in
      individuals without diabetes. We investigated the association of autonomic
      function with 5-year changes in glucose metabolism in individuals without
      diabetes. RESEARCH DESIGN AND METHODS: Analyses were based on 9,000
      person-examinations for 3,631 participants without diabetes in the Whitehall II
      cohort. Measures of autonomic function included 5-min resting heart rate and six 
      heart rate variability (HRV) indices. Associations between baseline autonomic
      function measures and 5-year changes in fasting and 2-h plasma glucose, serum
      insulin concentrations, insulin sensitivity (insulin sensitivity index [ISI0-120]
      and HOMA of insulin sensitivity), and beta-cell function (HOMA of beta-cell
      function) were estimated in models adjusting for age, sex, ethnicity, metabolic
      factors, and medication. RESULTS: A 10-bpm higher resting heart rate was
      associated with 5-year changes in fasting and 2-h insulin and ISI0-120 of 3.3%
      change (95% CI 1.8; 4.8)%, P < 0.001; 3.3% change (1.3; 5.3), P = 0.001; and -1.4
      (-2.4; -0.3), P = 0.009, respectively. In models adjusted for age, sex, and
      ethnicity, higher baseline values of several HRV indices were associated with a
      5-year decrease in fasting and 2-h insulin and ISI0-120. However, significance
      was lost by full adjustment. A majority of HRV indices exhibited a trend toward
      higher values being associated with lower insulin levels and higher insulin
      sensitivity. CONCLUSIONS: Higher resting heart rate in individuals without
      diabetes is associated with future unfavorable changes in insulin levels and
      insulin sensitivity. Associations may be mediated via autonomic function;
      however, results are inconclusive. Resting heart rate may be a risk marker for
      future pathophysiological changes in glucose metabolism.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Hansen, Christian Stevns
AU  - Hansen CS
AUID- ORCID: http://orcid.org/0000-0002-5782-3476
AD  - Steno Diabetes Center Copenhagen, Gentofte, Denmark
      christian.stevns.hansen@regionh.dk.
FAU - Faerch, Kristine
AU  - Faerch K
AUID- ORCID: http://orcid.org/0000-0002-6127-0448
AD  - Steno Diabetes Center Copenhagen, Gentofte, Denmark.
FAU - Jorgensen, Marit Eika
AU  - Jorgensen ME
AUID- ORCID: http://orcid.org/0000-0001-8356-5565
AD  - National Institute of Public Health, Southern Denmark University, Odense,
      Denmark.
FAU - Malik, Marek
AU  - Malik M
AD  - National Heart and Lung Institute, Imperial College, London, U.K.
FAU - Witte, Daniel R
AU  - Witte DR
AD  - Department of Public Health, Aarhus University, Aarhus, Denmark.
AD  - Danish Diabetes Academy, Odense, Denmark.
FAU - Brunner, Eric J
AU  - Brunner EJ
AD  - Department of Epidemiology and Public Health, University College London, London, 
      U.K.
FAU - Tabak, Adam G
AU  - Tabak AG
AD  - Department of Epidemiology and Public Health, University College London, London, 
      U.K.
AD  - Faculty of Medicine, Semmelweis University, Budapest, Hungary.
FAU - Kivimaki, Mika
AU  - Kivimaki M
AUID- ORCID: http://orcid.org/0000-0002-4699-5627
AD  - Department of Epidemiology and Public Health, University College London, London, 
      U.K.
FAU - Vistisen, Dorte
AU  - Vistisen D
AUID- ORCID: http://orcid.org/0000-0001-5045-5351
AD  - Steno Diabetes Center Copenhagen, Gentofte, Denmark.
LA  - eng
PT  - Journal Article
DEP - 20190402
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/04/04 06:00
MHDA- 2019/04/04 06:00
CRDT- 2019/04/04 06:00
PHST- 2018/08/31 00:00 [received]
PHST- 2019/01/22 00:00 [accepted]
PHST- 2019/04/04 06:00 [entrez]
PHST- 2019/04/04 06:00 [pubmed]
PHST- 2019/04/04 06:00 [medline]
AID - dc18-1838 [pii]
AID - 10.2337/dc18-1838 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Apr 2. pii: dc18-1838. doi: 10.2337/dc18-1838.

PMID- 30940641
OWN - NLM
STAT- Publisher
LR  - 20190403
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Apr 2
TI  - The Economic Burden of Elevated Blood Glucose Levels in 2017: Diagnosed and
      Undiagnosed Diabetes, Gestational Diabetes, and Prediabetes.
LID - dc181226 [pii]
LID - 10.2337/dc18-1226 [doi]
AB  - OBJECTIVE: This study was conducted to update national estimates of the economic 
      burden of undiagnosed diabetes, prediabetes, and gestational diabetes in the
      United States for year 2017 and provide state-level estimates. Combined with
      published estimates for diagnosed diabetes, these updated statistics provide a
      detailed picture of the economic costs associated with elevated blood glucose
      levels. RESEARCH DESIGN AND METHODS: This study estimated medical expenditures
      exceeding levels occurring in the absence of diabetes or prediabetes and the
      indirect economic burden associated with reduced labor force participation and
      productivity. Data sources analyzed included Optum medical claims for
      approximately 5.8 million commercially insured patients continuously enrolled
      from 2013 to 2015, Medicare Standard Analytical Files containing medical claims
      for approximately 2.8 million Medicare patients in 2014, and the 2014 Nationwide 
      Inpatient Sample containing approximately 7.1 million discharge records. Other
      data sources were the U.S. Census Bureau, Centers for Disease Control and
      Prevention, and Centers for Medicare and Medicaid Services. RESULTS: The economic
      burden associated with diagnosed diabetes (all ages), undiagnosed diabetes and
      prediabetes (adults), and gestational diabetes (mothers and newborns) reached
      nearly $404 billion in 2017, consisting of $327.2 billion for diagnosed diabetes,
      $31.7 billion for undiagnosed diabetes, $43.4 billion for prediabetes, and nearly
      $1.6 billion for gestational diabetes. Combined, this amounted to an economic
      burden of $1,240 for each American in 2017. Annual burden per case averaged
      $13,240 for diagnosed diabetes, $5,800 for gestational diabetes, $4,250 for
      undiagnosed diabetes, and $500 for prediabetes. CONCLUSIONS: Updated statistics
      underscore the importance of reducing the burden of prediabetes and diabetes
      through better detection, prevention, and treatment.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Dall, Timothy M
AU  - Dall TM
AUID- ORCID: http://orcid.org/0000-0001-5106-9401
AD  - IHS Markit, Washington, DC tim.dall@ihsmarkit.com.
FAU - Yang, Wenya
AU  - Yang W
AD  - Lewin Group, Falls Church, VA.
FAU - Gillespie, Karin
AU  - Gillespie K
AD  - Novo Nordisk, Plainsboro, NJ.
FAU - Mocarski, Michelle
AU  - Mocarski M
AD  - Novo Nordisk, Plainsboro, NJ.
FAU - Byrne, Erin
AU  - Byrne E
AD  - Novo Nordisk, Plainsboro, NJ.
FAU - Cintina, Inna
AU  - Cintina I
AD  - Lewin Group, Falls Church, VA.
FAU - Beronja, Kaleigh
AU  - Beronja K
AD  - Lewin Group, Falls Church, VA.
FAU - Semilla, April P
AU  - Semilla AP
AD  - IHS Markit, Washington, DC.
FAU - Iacobucci, William
AU  - Iacobucci W
AD  - IHS Markit, Washington, DC.
FAU - Hogan, Paul F
AU  - Hogan PF
AD  - Lewin Group, Falls Church, VA.
LA  - eng
PT  - Journal Article
DEP - 20190402
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/04/04 06:00
MHDA- 2019/04/04 06:00
CRDT- 2019/04/04 06:00
PHST- 2018/06/06 00:00 [received]
PHST- 2019/03/07 00:00 [accepted]
PHST- 2019/04/04 06:00 [entrez]
PHST- 2019/04/04 06:00 [pubmed]
PHST- 2019/04/04 06:00 [medline]
AID - dc18-1226 [pii]
AID - 10.2337/dc18-1226 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Apr 2. pii: dc18-1226. doi: 10.2337/dc18-1226.

PMID- 30940640
OWN - NLM
STAT- Publisher
LR  - 20190403
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Apr 2
TI  - Erratum. Secular TRends in DiabEtes in India (STRiDE-I): Change in Prevalence in 
      Ten Years Among Urban and Rural Populations in Tamil Nadu. Diabetes Care
      2019;42:476-485.
LID - dc19er06 [pii]
LID - 10.2337/dc19-er06 [doi]
FAU - Nanditha, Arun
AU  - Nanditha A
FAU - Snehalatha, Chamukuttan
AU  - Snehalatha C
FAU - Satheesh, Krishnamoorthy
AU  - Satheesh K
FAU - Susairaj, Priscilla
AU  - Susairaj P
FAU - Simon, Mary
AU  - Simon M
FAU - Vijaya, Lakshminarayanan
AU  - Vijaya L
FAU - Raghavan, Arun
AU  - Raghavan A
FAU - Vinitha, Ramachandran
AU  - Vinitha R
FAU - Ramachandran, Ambady
AU  - Ramachandran A
LA  - eng
PT  - Journal Article
PT  - Published Erratum
DEP - 20190402
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EFR - Diabetes Care. 2019 Mar;42(3):476-485. PMID: 30659076
EDAT- 2019/04/04 06:00
MHDA- 2019/04/04 06:00
CRDT- 2019/04/04 06:00
PHST- 2019/04/04 06:00 [entrez]
PHST- 2019/04/04 06:00 [pubmed]
PHST- 2019/04/04 06:00 [medline]
AID - dc19-er06 [pii]
AID - 10.2337/dc19-er06 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Apr 2. pii: dc19-er06. doi: 10.2337/dc19-er06.

PMID- 30936112
OWN - NLM
STAT- Publisher
LR  - 20190402
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Apr 1
TI  - Erratum. Urine Complement Proteins and the Risk of Kidney Disease Progression and
      Mortality in Type 2 Diabetes. Diabetes Care 2018;41:2361-2369.
LID - dc19er06a [pii]
LID - 10.2337/dc19-er06a [doi]
FAU - Vaisar, Tomas
AU  - Vaisar T
FAU - Durbin-Johnson, Blythe
AU  - Durbin-Johnson B
FAU - Whitlock, Kathryn
AU  - Whitlock K
FAU - Babenko, Ilona
AU  - Babenko I
FAU - Mehrotra, Rajnish
AU  - Mehrotra R
FAU - Rocke, David M
AU  - Rocke DM
FAU - Afkarian, Maryam
AU  - Afkarian M
LA  - eng
PT  - Journal Article
PT  - Published Erratum
DEP - 20190401
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EFR - Diabetes Care. 2018 Nov;41(11):2361-2369. PMID: 30150236
EDAT- 2019/04/03 06:00
MHDA- 2019/04/03 06:00
CRDT- 2019/04/03 06:00
PHST- 2019/04/03 06:00 [entrez]
PHST- 2019/04/03 06:00 [pubmed]
PHST- 2019/04/03 06:00 [medline]
AID - dc19-er06a [pii]
AID - 10.2337/dc19-er06a [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Apr 1. pii: dc19-er06a. doi: 10.2337/dc19-er06a.

PMID- 30936111
OWN - NLM
STAT- Publisher
LR  - 20190402
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Apr 1
TI  - Association Between Topical Corticosteroid Use and Type 2 Diabetes in Two
      European Population-Based Adult Cohorts.
LID - dc182158 [pii]
LID - 10.2337/dc18-2158 [doi]
AB  - OBJECTIVE: Topical corticosteroids (CSs) are commonly used to treat inflammatory 
      skin conditions including eczema and psoriasis. Although topical CS package
      inserts describe hyperglycemia and glycosuria as adverse drug reactions, it is
      unclear whether topical CS use in real life is also associated with an increased 
      risk of type 2 diabetes (T2D). RESEARCH DESIGN AND METHODS: Two matched
      case-control studies and one cohort study were conducted using routinely
      collected health care data from Denmark and the U.K. A total of 115,218 and
      54,944 adults were identified as case subjects with new-onset T2D in the Danish
      and U.K. case-control study, respectively. For the Danish cohort study, 2,689,473
      adults were included. The main exposure was topical CSs, and the outcome was
      incident T2D. RESULTS: Topical CS was significantly associated with T2D in the
      Danish (adjusted odds ratio [OR] 1.35 [95% CI 1.33-1.38]) and U.K. (adjusted OR
      1.23 [95% CI 1.19-1.27]) case-control studies. Individuals who were exposed to
      topical CSs had significantly increased risk of incident T2D (adjusted hazard
      ratio 1.27 [95% CI 1.26-1.29]). We observed significant dose-response
      relationships between T2D and increasing potency of topical CSs in the two Danish
      studies. The results were consistent across all sensitivity analyses.
      CONCLUSIONS: We found a positive association between topical CS prescribing and
      incident T2D in Danish and U.K. adult populations. Clinicians should be cognizant
      of possible diabetogenic effects of potent topical CSs.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Andersen, Yuki M F
AU  - Andersen YMF
AUID- ORCID: http://orcid.org/0000-0001-6131-2815
AD  - Department of Dermatology and Allergy, Herlev and Gentofte Hospital, University
      of Copenhagen, Hellerup, Denmark yuki.maria.fukuda.andersen.01@regionh.dk.
AD  - Copenhagen Research Group for Inflammatory Skin (CORGIS), Herlev and Gentofte
      Hospital, University of Copenhagen, Hellerup, Denmark.
AD  - Department of Cardiology, Herlev and Gentofte Hospital, University of Copenhagen,
      Hellerup, Denmark.
FAU - Egeberg, Alexander
AU  - Egeberg A
AD  - Department of Dermatology and Allergy, Herlev and Gentofte Hospital, University
      of Copenhagen, Hellerup, Denmark.
AD  - Copenhagen Research Group for Inflammatory Skin (CORGIS), Herlev and Gentofte
      Hospital, University of Copenhagen, Hellerup, Denmark.
FAU - Ban, Lu
AU  - Ban L
AD  - Centre of Evidence Based Dermatology, University of Nottingham, Nottingham, U.K.
AD  - NIHR Nottingham Biomedical Research Centre, Nottingham University Hospitals NHS
      Trust and the University of Nottingham, Nottingham, U.K.
FAU - Gran, Sonia
AU  - Gran S
AD  - Centre of Evidence Based Dermatology, University of Nottingham, Nottingham, U.K.
FAU - Williams, Hywel C
AU  - Williams HC
AD  - Centre of Evidence Based Dermatology, University of Nottingham, Nottingham, U.K.
FAU - Francis, Nick A
AU  - Francis NA
AD  - Division of Population Medicine, School of Medicine, Cardiff University, Cardiff,
      U.K.
FAU - Knop, Filip K
AU  - Knop FK
AUID- ORCID: http://orcid.org/0000-0002-2495-5034
AD  - Clinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte
      Hospital, University of Copenhagen, Hellerup, Denmark.
AD  - Department of Clinical Medicine, Faculty of Health and Medical Sciences,
      University of Copenhagen, Copenhagen, Denmark.
AD  - Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health
      and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
FAU - Gislason, Gunnar H
AU  - Gislason GH
AD  - Department of Cardiology, Herlev and Gentofte Hospital, University of Copenhagen,
      Hellerup, Denmark.
FAU - Skov, Lone
AU  - Skov L
AD  - Department of Dermatology and Allergy, Herlev and Gentofte Hospital, University
      of Copenhagen, Hellerup, Denmark.
AD  - Copenhagen Research Group for Inflammatory Skin (CORGIS), Herlev and Gentofte
      Hospital, University of Copenhagen, Hellerup, Denmark.
AD  - Department of Clinical Medicine, Faculty of Health and Medical Sciences,
      University of Copenhagen, Copenhagen, Denmark.
FAU - Thyssen, Jacob P
AU  - Thyssen JP
AD  - Department of Dermatology and Allergy, Herlev and Gentofte Hospital, University
      of Copenhagen, Hellerup, Denmark.
AD  - Copenhagen Research Group for Inflammatory Skin (CORGIS), Herlev and Gentofte
      Hospital, University of Copenhagen, Hellerup, Denmark.
AD  - Department of Clinical Medicine, Faculty of Health and Medical Sciences,
      University of Copenhagen, Copenhagen, Denmark.
LA  - eng
PT  - Journal Article
DEP - 20190401
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/04/03 06:00
MHDA- 2019/04/03 06:00
CRDT- 2019/04/03 06:00
PHST- 2018/10/15 00:00 [received]
PHST- 2019/03/07 00:00 [accepted]
PHST- 2019/04/03 06:00 [entrez]
PHST- 2019/04/03 06:00 [pubmed]
PHST- 2019/04/03 06:00 [medline]
AID - dc18-2158 [pii]
AID - 10.2337/dc18-2158 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Apr 1. pii: dc18-2158. doi: 10.2337/dc18-2158.

PMID- 30946456
OWN - NLM
STAT- Publisher
LR  - 20190404
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Apr 4
TI  - Effects of Diabetes on Motor Recovery after Cerebral Infarct: A Diffusion Tensor 
      Imaging Study.
LID - jc.2018-02502 [pii]
LID - 10.1210/jc.2018-02502 [doi]
AB  - PURPOSE: Little is known about the effects of diabetes on motor recovery after
      cerebral infarct. To address this, we recruited patients with corona radiata
      infarct and controlled for the integrity of the corticospinal tract (CST)
      determined using diffusion tensor tractography (DTT). METHODS: One hundred
      patients were recruited, and DTT was performed within 7-30 days of infarct onset.
      Based on the DTT findings (DTT+: CST was preserved around the infarct, DTT-: CST 
      was interrupted by the infarct) and the presence (DM+) or absence (DM-) of
      diabetes, patients were divided into, DTT+/DM- (36 patients), DTT+/DM+ (19
      patients), DTT-/DM- (32 patients), and DTT-/DM+ (13 patients) groups. Six months 
      after cerebral infarct, motor function on the affected side was evaluated for
      each patient using the upper Motricity Index (MI), lower MI, modified Brunnstrom 
      classification (MBC), and the functional ambulation category (FAC). RESULTS: In
      the patients with a DTT+ finding, no motor function scores were significantly
      different between the DTT+/DM- and DTT+/DM+ groups at six-month evaluation.
      However, in patients with DTT- finding, all motor function scores at the
      six-month evaluation were significantly higher in the DTT-/DM- group than in the 
      DTT-/DM+ group. CONCLUSION: When the CST is interrupted by a corona radiata
      infarct, recovery of motor function in patients with diabetes is more impaired
      than those without diabetes.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Moon, Jun Sung
AU  - Moon JS
AD  - Division of Endocrinology and Metabolism, Department of Internal Medicine,
      College of Medicine, Yeungnam University.
FAU - Chung, Seung Min
AU  - Chung SM
AD  - Division of Endocrinology and Metabolism, Department of Internal Medicine,
      College of Medicine, Yeungnam University.
FAU - Jang, Sung Ho
AU  - Jang SH
AD  - Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam
      University.
FAU - Won, Kyu Chang
AU  - Won KC
AD  - Division of Endocrinology and Metabolism, Department of Internal Medicine,
      College of Medicine, Yeungnam University.
FAU - Chang, Min Cheol
AU  - Chang MC
AD  - Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam
      University.
LA  - eng
PT  - Journal Article
DEP - 20190404
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/04/05 06:00
MHDA- 2019/04/05 06:00
CRDT- 2019/04/05 06:00
PHST- 2018/11/21 00:00 [received]
PHST- 2019/03/29 00:00 [accepted]
PHST- 2019/04/05 06:00 [entrez]
PHST- 2019/04/05 06:00 [pubmed]
PHST- 2019/04/05 06:00 [medline]
AID - 5426810 [pii]
AID - 10.1210/jc.2018-02502 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Apr 4. pii: 5426810. doi: 10.1210/jc.2018-02502.

PMID- 30938764
OWN - NLM
STAT- Publisher
LR  - 20190402
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Apr 2
TI  - Metformin Improves Peripheral Insulin Sensitivity in Youth with Type 1 Diabetes.
LID - jc.2019-00129 [pii]
LID - 10.1210/jc.2019-00129 [doi]
AB  - CONTEXT: Type 1 diabetes in adolescence is characterized by insulin deficiency
      and resistance (IR), both thought to increase cardiovascular disease risk. We
      previously demonstrated adolescents with type 1 diabetes have adipose, hepatic
      and muscle IR, and that metformin lowers daily insulin dose, suggesting improved 
      IR. However, whether metformin improves IR in muscle, hepatic or adipose tissues 
      in type 1 diabetes was unknown. OBJECTIVE: Measure peripheral, hepatic and
      adipose insulin sensitivity before and after metformin or placebo therapy in
      obese youth with type 1 diabetes. DESIGN: Double-blind placebo controlled
      clinical trial. SETTING: Multi-Center at 8 sites of the type 1 diabetes Exchange 
      Clinic Network. PATIENTS OR OTHER PARTICIPANTS: A subset of 12-19 year-olds with 
      type 1 diabetes (inclusion criteria: BMI >/=85th percentile, HbA1c 7.5-9.9%,
      insulin dosing >/=0.8 units/kg/day) from a larger trial (NCT02045290) were
      enrolled. INTERVENTION: Participants were randomized to 3 months of metformin
      (N=19) or placebo (N=18), underwent three-phase hyperinsulinemic euglycemic clamp
      with glucose and glycerol isotope tracers to assess tissue-specific IR before and
      after treatment. MAIN OUTCOME MEASURES: Peripheral insulin sensitivity,
      endogenous glucose release, rate of lipolysis. RESULTS: Between-group differences
      in change in insulin sensitivity favored metformin regarding whole-body IR
      (glucose infusion rate 1.3 [0.1, 2.4] mg/kg/min, p=0.03) and peripheral IR (
      metabolic clearance rate 0.923 [-0.002, 1.867] dL/kg/min, p=0.05). Metformin did 
      not impact insulin suppression of endogenous glucose release (p=0.12). Adipose IR
      was not assessable with traditional methods in this highly-IR population.
      CONCLUSIONS: Metformin appears to improve whole-body and peripheral IR in
      overweight/obese youth with type 1 diabetes.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Cree-Green, Melanie
AU  - Cree-Green M
AD  - Department of Pediatrics, Division of Pediatric Endocrinology, University of
      Colorado Anschutz Medical Campus, Aurora, CO.
AD  - Center for Women's Health Research, University of Colorado Anschutz Medical
      Campus, Aurora, CO.
FAU - Bergman, Bryan C
AU  - Bergman BC
AD  - Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism,
      University of Colorado Anschutz Medical Campus, Aurora, CO.
FAU - Cengiz, Eda
AU  - Cengiz E
AD  - Yale School of Medicine University.
FAU - Fox, Larry A
AU  - Fox LA
AD  - Nemours Children's Specialty Care, Jacksonville, FL.
FAU - Hannon, Tamara S
AU  - Hannon TS
AD  - Indiana University School of Medicine, Department of Pediatrics, Division of
      Pediatric Endocrinology & Diabetology.
FAU - Miller, Kellee
AU  - Miller K
AD  - Jaeb Center for Health Research, Tampa, FL.
FAU - Nathan, Brandon
AU  - Nathan B
AD  - University of Minnesota.
FAU - Pyle, Laura
AU  - Pyle L
AD  - Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora,
      CO.
AD  - Department of Biostatistics and Informatics, Colorado School of Public Health,
      University of Anschutz Medical Campus, Aurora, CO.
FAU - Kahn, Darcy
AU  - Kahn D
AD  - Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism,
      University of Colorado Anschutz Medical Campus, Aurora, CO.
FAU - Tansey, Michael
AU  - Tansey M
AD  - Department of Biostatistics and Informatics, Colorado School of Public Health,
      University of Anschutz Medical Campus, Aurora, CO.
FAU - Tichy, Eileen
AU  - Tichy E
AD  - Yale School of Medicine University.
FAU - Tsalikian, Eva
AU  - Tsalikian E
AD  - Department of Biostatistics and Informatics, Colorado School of Public Health,
      University of Anschutz Medical Campus, Aurora, CO.
FAU - Libman, Ingrid
AU  - Libman I
AD  - University of Iowa, Stead Family Department of Pediatrics, Endocrinology and
      Diabetes,.Children's Hospital of Pittsburgh at University of Pittsburgh Medical
      Center.
FAU - Nadeau, Kristen J
AU  - Nadeau KJ
AD  - Department of Pediatrics, Division of Pediatric Endocrinology, University of
      Colorado Anschutz Medical Campus, Aurora, CO.
AD  - Center for Women's Health Research, University of Colorado Anschutz Medical
      Campus, Aurora, CO.
AD  - Barbara Davis Center for Childhood Diabetes, University of Colorado Anschutz
      Medical Campus, Aurora, CO.
LA  - eng
SI  - ClinicalTrials.gov/NCT02045290
PT  - Journal Article
DEP - 20190402
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/04/03 06:00
MHDA- 2019/04/03 06:00
CRDT- 2019/04/03 06:00
PHST- 2019/01/16 00:00 [received]
PHST- 2019/03/27 00:00 [accepted]
PHST- 2019/04/03 06:00 [entrez]
PHST- 2019/04/03 06:00 [pubmed]
PHST- 2019/04/03 06:00 [medline]
AID - 5423566 [pii]
AID - 10.1210/jc.2019-00129 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Apr 2. pii: 5423566. doi: 10.1210/jc.2019-00129.

PMID- 30938762
OWN - NLM
STAT- Publisher
LR  - 20190402
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Apr 2
TI  - Reductions in insulin resistance are mediated primarily via weight loss in
      subjects with type 2 diabetes on semaglutide.
LID - jc.2018-02685 [pii]
LID - 10.1210/jc.2018-02685 [doi]
AB  - CONTEXT: Semaglutide, a once-weekly glucagon-like peptide 1 (GLP-1) analog
      approved for use in patients with type 2 diabetes (T2D), demonstrated superior
      body weight (BW) reductions and decreased insulin resistance (IR) vs comparators 
      across the SUSTAIN 1-3 clinical trials. OBJECTIVE: To investigate the
      relationship between IR and BW across the SUSTAIN 1-3 trials. DESIGN: Post hoc
      analysis of the SUSTAIN 1-3 trials. SETTING: 311 sites in 30 countries. Patients 
      or Other Participants: 2,432 subjects with T2D. INTERVENTIONS: Semaglutide 0.5 or
      1.0 mg, placebo or active comparator (sitagliptin 100 mg, exenatide extended
      release 2.0 mg). MAIN OUTCOME MEASURE: To assess the extent of the effect on IR
      that is mediated (indirect effect) and not mediated (direct effect) by the effect
      on BW. RESULTS: Across SUSTAIN 1-3, mean BW was significantly reduced with
      semaglutide 0.5 mg (3.7-4.3 kg; p<0.0001) and semaglutide 1.0 mg (4.5-6.1 kg;
      p<0.0001) vs comparators (1.0-1.9 kg). There were significantly greater
      reductions in IR with semaglutide 0.5 mg (27-36%) and semaglutide 1.0 mg (32-46%)
      vs comparators (17-28%). Greater reductions in BW were generally associated with 
      greater decreases in IR. The effect on IR was primarily mediated by weight loss
      (70-80% and 34-94%, respectively, for semaglutide 0.5 mg and 1.0 mg vs
      comparator). CONCLUSIONS: Semaglutide consistently reduced BW and IR in subjects 
      with T2D in SUSTAIN 1-3. In this analysis, IR improvement was positively
      associated with, and primarily mediated by, the effect of semaglutide on BW.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Fonseca, Vivian A
AU  - Fonseca VA
AD  - Tulane University Health Sciences Center, New Orleans, Louisiana, USA.
FAU - Capehorn, Matthew S
AU  - Capehorn MS
AD  - Rotherham Institute for Obesity, Clifton Medical Centre, Rotherham, UK.
FAU - Garg, Satish K
AU  - Garg SK
AD  - University of Colorado Denver, Denver, Colorado, USA.
FAU - Jodar Gimeno, Esteban
AU  - Jodar Gimeno E
AD  - Hospital Universitario Quiron Salud Madrid, Universidad Europea de Madrid,
      Madrid, Spain.
FAU - Hansen, Oluf Hoejbjerg
AU  - Hansen OH
AD  - Novo Nordisk A/S, Soborg, Denmark.
FAU - Holst, Anders Gaarsdal
AU  - Holst AG
AD  - Novo Nordisk A/S, Soborg, Denmark.
FAU - Nayak, Gurudutt
AU  - Nayak G
AD  - Novo Nordisk A/S, Soborg, Denmark.
FAU - Seufert, Jochen
AU  - Seufert J
AD  - University of Freiburg Medical Center, Medical Faculty, University of Freiburg,
      Freiburg, Germany.
LA  - eng
PT  - Journal Article
DEP - 20190402
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/04/03 06:00
MHDA- 2019/04/03 06:00
CRDT- 2019/04/03 06:00
PHST- 2018/12/12 00:00 [received]
PHST- 2019/03/27 00:00 [accepted]
PHST- 2019/04/03 06:00 [entrez]
PHST- 2019/04/03 06:00 [pubmed]
PHST- 2019/04/03 06:00 [medline]
AID - 5423568 [pii]
AID - 10.1210/jc.2018-02685 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Apr 2. pii: 5423568. doi: 10.1210/jc.2018-02685.

PMID- 30933282
OWN - NLM
STAT- Publisher
LR  - 20190401
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Apr 1
TI  - Gastric emptying in patients with well-controlled type 2 diabetes compared to
      non-diabetic young and older controls.
LID - jc.2018-02736 [pii]
LID - 10.1210/jc.2018-02736 [doi]
AB  - CONTEXT: Gastric emptying is a major determinant of postprandial glycaemia, and
      is often delayed in longstanding, complicated type 2 diabetes (T2DM). There is,
      however, little information about gastric emptying in well-controlled T2DM.
      OBJECTIVE: To evaluate the rate of gastric emptying in community-based patients
      with relatively well-controlled T2DM, compared to non-diabetic young and older
      controls. PARTICIPANTS AND DESIGN: 111 patients with T2DM managed by diet (n=52) 
      or metformin monotherapy (n=59) (HbA1c 6.6+/-0.1%/49.0+/-0.9mmol/mol), 18 age-
      and BMI-matched older non-diabetic subjects, and 15 young healthy subjects
      consumed a standardised mashed potato meal (368.5kcal) containing 100uL
      13C-octanoic acid. Gastric emptying (by breath test) and blood glucose were
      evaluated over 240min. RESULTS: Gastric emptying was slower in the non-diabetic
      older than young subjects (2.3+/-0.1 vs. 3.0+/-0.1kcal/min, P=0.0008). However,
      relative to the age-/BMI-matched non-diabetic subjects, gastric emptying
      (2.8+/-0.1kcal/min) was faster in T2DM patients (P=0.0005). Furthermore, gastric 
      emptying was faster in the metformin-treated (3.0+/-0.1kcal/min) than
      diet-controlled (2.7+/-0.1kcal/min) T2DM patients (P=0.011), although there were 
      no differences in age, BMI, HbA1c or the duration of known diabetes. The
      increments in blood glucose (at t=30 and 60 and the incremental area under the
      curve during t=0-120min) after the meal were related directly to the rate of
      gastric emptying in the T2DM subjects, regardless of treatment with or without
      metformin (P<0.05 each). CONCLUSIONS: Gastric emptying is slowed with aging, but 
      otherwise is relatively more rapid in patients with well-controlled T2DM. This
      provides a strong rationale for slowing gastric emptying to improve postprandial 
      glycaemic control in these patients.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Watson, Linda E
AU  - Watson LE
AD  - Adelaide Medical School and Centre of Research Excellence (CRE) in Translating
      Nutritional Science to Good Health, The University of Adelaide, Adelaide,
      Australia.
FAU - Xie, Cong
AU  - Xie C
AD  - Adelaide Medical School and Centre of Research Excellence (CRE) in Translating
      Nutritional Science to Good Health, The University of Adelaide, Adelaide,
      Australia.
FAU - Wang, Xuyi
AU  - Wang X
AD  - Adelaide Medical School and Centre of Research Excellence (CRE) in Translating
      Nutritional Science to Good Health, The University of Adelaide, Adelaide,
      Australia.
AD  - Department of Endocrinology, Zhongda Hospital, Institute of Diabetes, School of
      Medicine, Southeast University, Nanjing, China.
FAU - Li, Ziyi
AU  - Li Z
AD  - Adelaide Medical School and Centre of Research Excellence (CRE) in Translating
      Nutritional Science to Good Health, The University of Adelaide, Adelaide,
      Australia.
FAU - Phillips, Liza K
AU  - Phillips LK
AD  - Adelaide Medical School and Centre of Research Excellence (CRE) in Translating
      Nutritional Science to Good Health, The University of Adelaide, Adelaide,
      Australia.
FAU - Sun, Zilin
AU  - Sun Z
AD  - Department of Endocrinology, Zhongda Hospital, Institute of Diabetes, School of
      Medicine, Southeast University, Nanjing, China.
FAU - Jones, Karen L
AU  - Jones KL
AD  - Adelaide Medical School and Centre of Research Excellence (CRE) in Translating
      Nutritional Science to Good Health, The University of Adelaide, Adelaide,
      Australia.
AD  - Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, Australia.
FAU - Horowitz, Michael
AU  - Horowitz M
AD  - Adelaide Medical School and Centre of Research Excellence (CRE) in Translating
      Nutritional Science to Good Health, The University of Adelaide, Adelaide,
      Australia.
AD  - Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, Australia.
FAU - Rayner, Christopher K
AU  - Rayner CK
AD  - Adelaide Medical School and Centre of Research Excellence (CRE) in Translating
      Nutritional Science to Good Health, The University of Adelaide, Adelaide,
      Australia.
FAU - Wu, Tongzhi
AU  - Wu T
AD  - Adelaide Medical School and Centre of Research Excellence (CRE) in Translating
      Nutritional Science to Good Health, The University of Adelaide, Adelaide,
      Australia.
AD  - Department of Endocrinology, Zhongda Hospital, Institute of Diabetes, School of
      Medicine, Southeast University, Nanjing, China.
AD  - Endocrine and Metabolic Unit, Royal Adelaide Hospital, Adelaide, Australia.
LA  - eng
PT  - Journal Article
DEP - 20190401
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/04/02 06:00
MHDA- 2019/04/02 06:00
CRDT- 2019/04/02 06:00
PHST- 2019/04/02 06:00 [entrez]
PHST- 2019/04/02 06:00 [pubmed]
PHST- 2019/04/02 06:00 [medline]
AID - 5421617 [pii]
AID - 10.1210/jc.2018-02736 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Apr 1. pii: 5421617. doi: 10.1210/jc.2018-02736.

PMID- 30938304
OWN - NLM
STAT- In-Data-Review
LR  - 20190402
IS  - 1474-547X (Electronic)
IS  - 0140-6736 (Linking)
VI  - 393
IP  - 10178
DP  - 2019 Mar 30
TI  - Gestational diabetes in England: cause for concern.
PG  - 1262
LID - S0140-6736(19)30741-X [pii]
LID - 10.1016/S0140-6736(19)30741-X [doi]
FAU - The Lancet
AU  - The Lancet
LA  - eng
PT  - Editorial
PL  - England
TA  - Lancet
JT  - Lancet (London, England)
JID - 2985213R
EDAT- 2019/04/03 06:00
MHDA- 2019/04/03 06:00
CRDT- 2019/04/03 06:00
PHST- 2019/04/03 06:00 [entrez]
PHST- 2019/04/03 06:00 [pubmed]
PHST- 2019/04/03 06:00 [medline]
AID - S0140-6736(19)30741-X [pii]
AID - 10.1016/S0140-6736(19)30741-X [doi]
PST - ppublish
SO  - Lancet. 2019 Mar 30;393(10178):1262. doi: 10.1016/S0140-6736(19)30741-X.