PMID- 29120506
OWN - NLM
STAT- MEDLINE
DCOM- 20180731
LR  - 20180815
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 35
IP  - 1
DP  - 2018 Jan
TI  - History of mood or anxiety disorders and risk of gestational diabetes mellitus in
      a population-based cohort.
PG  - 147-151
LID - 10.1111/dme.13543 [doi]
AB  - AIM: To examine the association between mood and anxiety disorders and the
      development of gestational diabetes mellitus in a retrospective population-based 
      cohort study. METHODS: Clinical data from a provincial perinatal health registry 
      were linked to physician claims, hospitalization records and emergency visits to 
      identify any diagnoses of mood or anxiety disorders in the 2 years prior to
      pregnancy and a subsequent diagnosis of gestational diabetes during pregnancy.
      The study population included all singleton pregnancies in the Canadian province 
      of Alberta from 1 April 2000 to 31 March 2010. Generalized estimating equations
      were used to determine the adjusted odds ratio of gestational diabetes, comparing
      women with and without a history of mood or anxiety disorders. RESULTS: Among 373
      674 pregnancies from 253 911 women, 25.7% had a history of mood or anxiety
      disorders, and 3.8% developed gestational diabetes. The multivariate-adjusted
      odds of developing gestational diabetes were higher among women with a history of
      mood or anxiety disorders (odds ratio 1.10, 95% CI 1.06-1.14). CONCLUSIONS: Women
      with a history of mood or anxiety disorders had a moderately increased risk of
      developing gestational diabetes.
CI  - (c) 2017 Diabetes UK.
FAU - Beka, Q
AU  - Beka Q
AD  - School of Public Health, University of Alberta, Edmonton, Canada.
FAU - Bowker, S L
AU  - Bowker SL
AD  - School of Public Health, University of Alberta, Edmonton, Canada.
FAU - Savu, A
AU  - Savu A
AUID- ORCID: 0000-0001-8070-4195
AD  - Department of Medicine, University of Alberta, Edmonton, Canada.
FAU - Kingston, D
AU  - Kingston D
AD  - Faculty of Nursing, University of Calgary, Calgary, Alberta, Canada.
FAU - Johnson, J A
AU  - Johnson JA
AD  - School of Public Health, University of Alberta, Edmonton, Canada.
FAU - Kaul, P
AU  - Kaul P
AUID- ORCID: 0000-0003-2239-3944
AD  - Department of Medicine, University of Alberta, Edmonton, Canada.
LA  - eng
GR  - CIHR/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
SB  - IM
MH  - Adult
MH  - Alberta/epidemiology
MH  - Anxiety Disorders/*epidemiology
MH  - Cohort Studies
MH  - Diabetes, Gestational/*epidemiology
MH  - Female
MH  - Humans
MH  - Mood Disorders/*epidemiology
MH  - Multivariate Analysis
MH  - Odds Ratio
MH  - Pregnancy
MH  - Retrospective Studies
MH  - Risk Factors
MH  - Young Adult
EDAT- 2017/11/10 06:00
MHDA- 2018/08/01 06:00
CRDT- 2017/11/10 06:00
PHST- 2017/11/01 00:00 [accepted]
PHST- 2017/11/10 06:00 [pubmed]
PHST- 2018/08/01 06:00 [medline]
PHST- 2017/11/10 06:00 [entrez]
AID - 10.1111/dme.13543 [doi]
PST - ppublish
SO  - Diabet Med. 2018 Jan;35(1):147-151. doi: 10.1111/dme.13543.

PMID- 29120503
OWN - NLM
STAT- MEDLINE
DCOM- 20180731
LR  - 20180815
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 35
IP  - 1
DP  - 2018 Jan
TI  - Route to improving Type 1 diabetes mellitus glycaemic outcomes: real-world
      evidence taken from the National Diabetes Audit.
PG  - 63-71
LID - 10.1111/dme.13541 [doi]
AB  - AIM: To use general practice-level data for England, available through the
      National Diabetes Audit, and primary care prescribing data to identify
      prescription treatment factors associated with variations in achieved glucose
      control (HbA1c ). METHODS: General practice-level National Diabetes Audit data on
      Type 1 diabetes, including details of population characteristics, services,
      proportion of people achieving target glycaemic control [HbA1c </=58 mmol/mol
      (7.5%)] and proportion of people at high glycaemic risk [HbA1c >86 mmol/ml
      (10%)], were linked to 2013-2016 primary care diabetes prescribing data on
      insulin types and blood glucose monitoring for all people with diabetes. RESULTS:
      A wide variation was found between the 10(th) percentile and the 90(th)
      percentile of general practices in both target glycaemic control (15.6% to 44.8%,
      respectively) and high glycaemic risk (4.8% to 28.6%, respectively). Our analysis
      suggests that, given the extrapolated total of 280 000 people with Type 1
      diabetes in the UK, there may be the potential to increase the number of those
      within target glycaemic control from 80 000 to 101 000; 53% of this increase (11 
      000 people) would result from service improvements and 47% (10 000 people) from
      medication and technology changes. The same improvements would also provide the
      opportunity to reduce the number of people at high glycaemic risk from 42 000 to 
      26 500. A key factor associated with practice-level target HbA1c achievement
      would be greater use of insulin pumps for up to an additional 56 000 people.
      CONCLUSION: If the HbA1c achievement rates in service provision, medication and
      use of technology currently seen in practices in the 90(th) percentile were to be
      matched with regard to HbA1c achievement rates in all general practices,
      glycaemic control might be improved for 36 500 people, with all the attendant
      health benefits.
CI  - (c) 2017 Diabetes UK.
FAU - Heald, A H
AU  - Heald AH
AD  - School of Medicine and Manchester Academic Health Sciences Centre, University of 
      Manchester, Manchester, UK.
AD  - Department of Diabetes and Endocrinology, Salford Royal Hospital, Salford, UK.
FAU - Livingston, M
AU  - Livingston M
AD  - Department of Blood Sciences, Walsall Manor Hospital, Walsall, UK.
FAU - Fryer, A
AU  - Fryer A
AD  - Institute for Applied Clinical Sciences, Keele University, Keele, UK.
FAU - Moreno, G Y C
AU  - Moreno GYC
AUID- ORCID: 0000-0002-4506-8223
AD  - Co-ordinator of the Obesity Clinic in the Medicine School of Instituto
      Politecnico Nacional, Mexico City, Mexico.
FAU - Malipatil, N
AU  - Malipatil N
AD  - School of Medicine and Manchester Academic Health Sciences Centre, University of 
      Manchester, Manchester, UK.
FAU - Gadsby, R
AU  - Gadsby R
AD  - Warwick Medical School, University of Warwick, Coventry, UK.
FAU - Ollier, W
AU  - Ollier W
AD  - School of Medicine and Manchester Academic Health Sciences Centre, University of 
      Manchester, Manchester, UK.
FAU - Lunt, M
AU  - Lunt M
AD  - School of Medicine and Manchester Academic Health Sciences Centre, University of 
      Manchester, Manchester, UK.
FAU - Stedman, M
AU  - Stedman M
AD  - RES Consortium, Andover, Wiltshire, UK.
FAU - Young, R J
AU  - Young RJ
AD  - National Diabetes Audit, Central Office Diabetes UK, London, UK.
LA  - eng
GR  - G0900753/Medical Research Council/United Kingdom
GR  - MR/K002279/1/Medical Research Council/United Kingdom
GR  - G0600237/Medical Research Council/United Kingdom
GR  - G0100594/Medical Research Council/United Kingdom
GR  - G0901461/Medical Research Council/United Kingdom
PT  - Journal Article
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
RN  - 0 (Blood Glucose)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
RN  - 0 (hemoglobin A1c protein, human)
SB  - IM
CIN - Diabet Med. 2018 Jan;35(1):10-11. PMID: 29117449
MH  - Blood Glucose/metabolism
MH  - Blood Glucose Self-Monitoring
MH  - Diabetes Mellitus, Type 1/*drug therapy/metabolism
MH  - England
MH  - Glycated Hemoglobin A/*metabolism
MH  - Humans
MH  - Hypoglycemic Agents/*administration & dosage/therapeutic use
MH  - Insulin/*administration & dosage/therapeutic use
MH  - Insulin Infusion Systems
MH  - Medical Audit
MH  - Practice Patterns, Physicians'/*statistics & numerical data
MH  - *Primary Health Care
MH  - Quality Improvement
MH  - Treatment Outcome
EDAT- 2017/11/10 06:00
MHDA- 2018/08/01 06:00
CRDT- 2017/11/10 06:00
PHST- 2017/10/31 00:00 [accepted]
PHST- 2017/11/10 06:00 [pubmed]
PHST- 2018/08/01 06:00 [medline]
PHST- 2017/11/10 06:00 [entrez]
AID - 10.1111/dme.13541 [doi]
PST - ppublish
SO  - Diabet Med. 2018 Jan;35(1):63-71. doi: 10.1111/dme.13541.

PMID- 29117449
OWN - NLM
STAT- MEDLINE
DCOM- 20180816
LR  - 20180816
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 35
IP  - 1
DP  - 2018 Jan
TI  - Better uptake of technology and improved outcomes in Type 1 diabetes.
PG  - 10-11
LID - 10.1111/dme.13545 [doi]
FAU - Hammond, P J
AU  - Hammond PJ
AUID- ORCID: 0000-0001-5762-1084
AD  - Diabetes Resource Centre, Harrogate District Hospital, Harrogate, UK.
LA  - eng
PT  - Journal Article
PT  - Comment
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
SB  - IM
CON - Diabet Med. 2018 Jan;35(1):63-71. PMID: 29120503
MH  - *Diabetes Mellitus, Type 1
MH  - Humans
EDAT- 2017/11/09 06:00
MHDA- 2018/08/17 06:00
CRDT- 2017/11/09 06:00
PHST- 2017/11/02 00:00 [accepted]
PHST- 2017/11/09 06:00 [pubmed]
PHST- 2018/08/17 06:00 [medline]
PHST- 2017/11/09 06:00 [entrez]
AID - 10.1111/dme.13545 [doi]
PST - ppublish
SO  - Diabet Med. 2018 Jan;35(1):10-11. doi: 10.1111/dme.13545.

PMID- 29117445
OWN - NLM
STAT- In-Process
LR  - 20180815
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 35
IP  - 2
DP  - 2018 Feb
TI  - Intrapartum glycaemic control and neonatal hypoglycaemia in pregnancies
      complicated by diabetes: a systematic review.
PG  - 173-183
LID - 10.1111/dme.13546 [doi]
AB  - AIMS: To examine whether, in neonates of mothers with Type 1, Type 2 and
      gestational diabetes, in-target intrapartum glycaemic control was associated with
      a lower risk of neonatal hypoglycaemia compared with out-of-target glycaemic
      control. METHODS: We searched PubMed and EMBASE for all available publications,
      regardless of year, based on a published protocol (PROSPERO CRD42016052439).
      Studies were excluded if they did not report original data or were animal
      studies. Data were extracted from published reports in duplicate using a
      prespecified data extraction form. The main outcome of interest was the
      association between in-target intrapartum glycaemic control and neonatal
      hypoglycaemia. RESULTS: We screened 2846 records for potential study inclusion;
      23 studies, including approximately 2835 women with diabetes, were included in
      the systematic review. Only two of those studies specifically examined in-target 
      vs out-of-target intrapartum glycaemic control. Of the studies included, six
      showed a relationship between intrapartum glucose and neonatal hypoglycaemia,
      five others showed a relationship in at least one of the analyses performed and
      12 did not find a significant relationship. Only one study was identified as
      having a low risk of bias. CONCLUSIONS: There is a paucity of high-quality data
      supporting the association of glucose during labour and delivery with neonatal
      hypoglycaemia in pregnancies complicated by diabetes. Further studies are
      required to examine the impact of tight glycaemic targets in labour.
CI  - (c) 2017 Diabetes UK.
FAU - Yamamoto, J M
AU  - Yamamoto JM
AUID- ORCID: 0000-0002-3556-0820
AD  - Department of Medicine, University of Calgary, Calgary, Alberta, Canada.
FAU - Benham, J
AU  - Benham J
AD  - Department of Medicine, University of Calgary, Calgary, Alberta, Canada.
FAU - Mohammad, K
AU  - Mohammad K
AD  - Department of Pediatrics, University of Calgary, Calgary, Alberta, Canada.
FAU - Donovan, L E
AU  - Donovan LE
AD  - Department of Medicine, University of Calgary, Calgary, Alberta, Canada.
AD  - Department of Obstetrics and Gynecology, University of Calgary, Calgary, Alberta,
      Canada.
FAU - Wood, S
AU  - Wood S
AD  - Department of Obstetrics and Gynecology, University of Calgary, Calgary, Alberta,
      Canada.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
CIN - Diabet Med. 2018 Feb;35(2):159. PMID: 29333703
CIN - Diabet Med. 2018 Aug;35(8):1130-1131. PMID: 29719065
EDAT- 2017/11/09 06:00
MHDA- 2017/11/09 06:00
CRDT- 2017/11/09 06:00
PHST- 2017/11/03 00:00 [accepted]
PHST- 2017/11/09 06:00 [pubmed]
PHST- 2017/11/09 06:00 [medline]
PHST- 2017/11/09 06:00 [entrez]
AID - 10.1111/dme.13546 [doi]
PST - ppublish
SO  - Diabet Med. 2018 Feb;35(2):173-183. doi: 10.1111/dme.13546.

PMID- 29111600
OWN - NLM
STAT- MEDLINE
DCOM- 20180731
LR  - 20180815
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 35
IP  - 1
DP  - 2018 Jan
TI  - Mortality and acute complications in children and young adults diagnosed with
      Type 1 diabetes in Yorkshire, UK: a cohort study.
PG  - 112-120
LID - 10.1111/dme.13544 [doi]
AB  - AIMS: To examine all-cause and cause-specific mortality in a population-based
      cohort of people with early and late onset of Type 1 diabetes. METHODS: The
      Yorkshire Register of Diabetes in Children and Young People includes individuals 
      with early (0-14 years) and late (15-29 years) Type 1 diabetes onset, diagnosed
      between 1978 and 2013. This register was linked to death certification data from 
      the Office for National Statistics to calculate standardized mortality ratios,
      cumulative mortality curves using Kaplan-Meier survival estimates, and Cox
      regression modelling. Ethnicity was derived using Onomap. Deprivation status was 
      classified using the Townsend index. The underlying cause of death in each case
      was clinically verified. RESULTS: There were 229 deaths in 5498 individuals with 
      100 959 person-years of follow-up. The overall standardized mortality ratio was
      4.3 (95% CI 3.8 to 4.9). There were no significant differences in standardized
      mortality ratios according to age of onset, sex or deprivation status. The
      standardized mortality ratios were significantly higher for people of white
      ethnic origin [8.1 (95% CI 6.9 to 9.4)] than for those of South-Asian ethnic
      origin [3.4 (95% CI 1.7 to 6.4)]. The mortality risk was lower in those diagnosed
      in later years (2002 to 2013 for the early-onset and 2006 to 2013 for the
      late-onset group) compared with earlier years (1991 to 1997 for the early-onset
      and 1991 to 1997 for the late-onset group) for both onset groups [hazard ratio
      0.13 (95% CI 0.05 to 0.33) vs 0.24 (95% CI 0.07 to 0.81)]. Mortality risk
      improved over time for chronic complications in the early-onset group only, but
      there was no improvement in either onset group with regard to acute
      complications. CONCLUSIONS: An excess of deaths in the population with Type 1
      diabetes remains. Although the all-cause mortality risk has fallen over time, no 
      improvement has been found in the mortality risk associated with acute
      complications.
CI  - (c) 2017 Diabetes UK.
FAU - Evans-Cheung, T C
AU  - Evans-Cheung TC
AUID- ORCID: 0000-0003-0899-5383
AD  - Division of Epidemiology and Biostatistics, School of Medicine, University of
      Leeds, Leeds, UK.
FAU - Bodansky, H J
AU  - Bodansky HJ
AD  - Division of Epidemiology and Biostatistics, School of Medicine, University of
      Leeds, Leeds, UK.
AD  - Leeds Teaching Hospitals NHS Trust, Leeds, UK.
FAU - Parslow, R C
AU  - Parslow RC
AD  - Division of Epidemiology and Biostatistics, School of Medicine, University of
      Leeds, Leeds, UK.
FAU - Feltbower, R G
AU  - Feltbower RG
AD  - Division of Epidemiology and Biostatistics, School of Medicine, University of
      Leeds, Leeds, UK.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
SB  - IM
MH  - Acute Disease
MH  - Adolescent
MH  - Adult
MH  - Age of Onset
MH  - Asian Continental Ancestry Group/statistics & numerical data
MH  - Cause of Death
MH  - Child
MH  - Child, Preschool
MH  - Cohort Studies
MH  - Diabetes Complications/*mortality
MH  - Diabetes Mellitus, Type 1/*mortality
MH  - Ethnic Groups/statistics & numerical data
MH  - European Continental Ancestry Group/statistics & numerical data
MH  - Female
MH  - Humans
MH  - Infant
MH  - Infant, Newborn
MH  - Kaplan-Meier Estimate
MH  - Male
MH  - Middle Aged
MH  - Mortality
MH  - Proportional Hazards Models
MH  - *Registries
MH  - Social Class
MH  - United Kingdom/epidemiology
MH  - Young Adult
EDAT- 2017/11/08 06:00
MHDA- 2018/08/01 06:00
CRDT- 2017/11/08 06:00
PHST- 2017/11/01 00:00 [accepted]
PHST- 2017/11/08 06:00 [pubmed]
PHST- 2018/08/01 06:00 [medline]
PHST- 2017/11/08 06:00 [entrez]
AID - 10.1111/dme.13544 [doi]
PST - ppublish
SO  - Diabet Med. 2018 Jan;35(1):112-120. doi: 10.1111/dme.13544.

PMID- 29108100
OWN - NLM
STAT- MEDLINE
DCOM- 20180731
LR  - 20180815
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 35
IP  - 1
DP  - 2018 Jan
TI  - Association between diabetes mellitus and olfactory dysfunction: current
      perspectives and future directions.
PG  - 41-52
LID - 10.1111/dme.13542 [doi]
AB  - The increasing global prevalence of diabetes mellitus presents a significant
      challenge to healthcare systems today. Although diabetic retinopathy, nephropathy
      and neuropathy are well-established complications of diabetes, there is a paucity
      of research examining the impact of dysglycaemia on the olfactory system.
      Olfaction is an important sense, playing a role in the safety, nutrition and
      quality of life of an individual, but its importance is often overlooked when
      compared with the other senses. As a result, olfactory dysfunction is often
      underdiagnosed. The present review article aims to present and discuss the
      available evidence on the relationship between diabetes and olfaction. It also
      explores the associations between olfactory dysfunction and diabetes
      complications that could explain the underlying pathogenesis. Finally, it
      summarizes the putative pathological mechanisms underlying olfactory dysfunction 
      in diabetes that require further investigation.
CI  - (c) 2017 Diabetes UK.
FAU - Zaghloul, H
AU  - Zaghloul H
AD  - Clinical Research Core, Weill Cornell Medicine, Doha, Qatar.
AD  - Department of Medicine, Weill Cornell Medicine, Doha, Qatar.
AD  - Weill Cornell Medicine, New York, NY, USA.
FAU - Pallayova, M
AU  - Pallayova M
AD  - Clinical Research Core, Weill Cornell Medicine, Doha, Qatar.
AD  - Department of Medicine, Weill Cornell Medicine, Doha, Qatar.
AD  - Weill Cornell Medicine, New York, NY, USA.
FAU - Al-Nuaimi, O
AU  - Al-Nuaimi O
AD  - Carnegie Mellon University, Doha, Qatar.
AD  - Carnegie Mellon University, Pittsburgh, PA, USA.
FAU - Hovis, K R
AU  - Hovis KR
AD  - Carnegie Mellon University, Doha, Qatar.
AD  - Carnegie Mellon University, Pittsburgh, PA, USA.
FAU - Taheri, S
AU  - Taheri S
AUID- ORCID: 0000-0001-8314-1500
AD  - Clinical Research Core, Weill Cornell Medicine, Doha, Qatar.
AD  - Department of Medicine, Weill Cornell Medicine, Doha, Qatar.
AD  - Weill Cornell Medicine, New York, NY, USA.
LA  - eng
PT  - Journal Article
PT  - Review
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
SB  - IM
MH  - Albuminuria/epidemiology
MH  - Diabetes Complications/*epidemiology/metabolism/physiopathology
MH  - Diabetes Mellitus/*epidemiology/metabolism/physiopathology
MH  - Diabetic Nephropathies/epidemiology
MH  - Diabetic Neuropathies/epidemiology
MH  - Humans
MH  - Olfaction Disorders/*epidemiology/metabolism/physiopathology
MH  - Oxidative Stress
EDAT- 2017/11/07 06:00
MHDA- 2018/08/01 06:00
CRDT- 2017/11/07 06:00
PHST- 2017/10/31 00:00 [accepted]
PHST- 2017/11/07 06:00 [pubmed]
PHST- 2018/08/01 06:00 [medline]
PHST- 2017/11/07 06:00 [entrez]
AID - 10.1111/dme.13542 [doi]
PST - ppublish
SO  - Diabet Med. 2018 Jan;35(1):41-52. doi: 10.1111/dme.13542.

PMID- 29109245
OWN - NLM
STAT- Publisher
LR  - 20180202
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2017 Nov 6
TI  - Expression of Concern. Protein Kinase C (PKC)-alpha Activation Inhibits PKC-zeta 
      and Mediates the Action of PED/PEA-15 on Glucose Transport in the L6 Skeletal
      Muscle Cells. Diabetes 2001;50:1244-1252. DOI:
      https://doi.org/10.2337/diabetes.50.6.1244. PMID: 11375323.
LID - db17ec2017b [pii]
LID - 10.2337/db17-ec2017b [doi]
FAU - Condorelli, Gerolama
AU  - Condorelli G
FAU - Vigliotta, Giovanni
AU  - Vigliotta G
FAU - Trencia, Alessandra
AU  - Trencia A
FAU - Maitan, Maria Alessandra
AU  - Maitan MA
FAU - Caruso, Matilde
AU  - Caruso M
FAU - Miele, Claudia
AU  - Miele C
FAU - Oriente, Francesco
AU  - Oriente F
FAU - Santopietro, Stefania
AU  - Santopietro S
FAU - Formisano, Pietro
AU  - Formisano P
FAU - Beguinot, Francesco
AU  - Beguinot F
LA  - eng
PT  - Journal Article
PT  - Expression of Concern
DEP - 20171106
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
ECF - Diabetes. 2001 Jun;50(6):1244-52. PMID: 11375323
PMC - PMC5780058
EDAT- 2017/11/08 06:00
MHDA- 2017/11/08 06:00
CRDT- 2017/11/08 06:00
PMCR- 2019/02/01 00:00
PHST- 2019/02/01 00:00 [pmc-release]
PHST- 2017/11/08 06:00 [entrez]
PHST- 2017/11/08 06:00 [pubmed]
PHST- 2017/11/08 06:00 [medline]
AID - db17-ec2017b [pii]
AID - 10.2337/db17-ec2017b [doi]
PST - aheadofprint
SO  - Diabetes. 2017 Nov 6. pii: db17-ec2017b. doi: 10.2337/db17-ec2017b.

PMID- 29109244
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20180514
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
VI  - 67
IP  - 2
DP  - 2018 Feb
TI  - Expression of Concern. Prep1 Controls Insulin Glucoregulatory Function in Liver
      by Transcriptional Targeting of SHP1 Tyrosine Phosphatase. Diabetes
      2011;60:138-147. DOI: 10.2337/db10-0860. PMID: 20864515.
PG  - 346-347
LID - 10.2337/db17-ec2017c [doi]
FAU - Oriente, Francesco
AU  - Oriente F
FAU - Iovino, Salvatore
AU  - Iovino S
FAU - Cabaro, Serena
AU  - Cabaro S
FAU - Cassese, Angela
AU  - Cassese A
FAU - Longobardi, Elena
AU  - Longobardi E
FAU - Miele, Claudia
AU  - Miele C
FAU - Ungaro, Paola
AU  - Ungaro P
FAU - Formisano, Pietro
AU  - Formisano P
FAU - Blasi, Francesco
AU  - Blasi F
FAU - Beguinot, Francesco
AU  - Beguinot F
LA  - eng
PT  - Journal Article
PT  - Expression of Concern
DEP - 20171106
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
ECF - Diabetes. 2011 Jan;60(1):138-47. PMID: 20864515
PMC - PMC5780057
EDAT- 2017/11/08 06:00
MHDA- 2017/11/08 06:01
CRDT- 2017/11/08 06:00
PHST- 2017/11/08 06:00 [pubmed]
PHST- 2017/11/08 06:01 [medline]
PHST- 2017/11/08 06:00 [entrez]
AID - db17-ec2017c [pii]
AID - 10.2337/db17-ec2017c [doi]
PST - ppublish
SO  - Diabetes. 2018 Feb;67(2):346-347. doi: 10.2337/db17-ec2017c. Epub 2017 Nov 6.

PMID- 29109243
OWN - NLM
STAT- Publisher
LR  - 20180202
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2017 Nov 6
TI  - Expression of Concern. The IR1152 Mutant Insulin Receptor Selectively Impairs
      Insulin Action in Skeletal Muscle but Not in Liver. Diabetes 2000;49:1194-1202.
      DOI: https://doi.org/10.2337/diabetes.49.7.1194. PMID: 10909978.
LID - db17ec2017a [pii]
LID - 10.2337/db17-ec2017a [doi]
FAU - Caruso, Matilde
AU  - Caruso M
FAU - Miele, Claudia
AU  - Miele C
FAU - Oliva, Andrea
AU  - Oliva A
FAU - Condorelli, Gerolama
AU  - Condorelli G
FAU - Oriente, Francesco
AU  - Oriente F
FAU - Riccardi, Gabriele
AU  - Riccardi G
FAU - Capaldo, Brunella
AU  - Capaldo B
FAU - Fiory, Francesca
AU  - Fiory F
FAU - Accili, Domenico
AU  - Accili D
FAU - Formisano, Pietro
AU  - Formisano P
FAU - Beguinot, Francesco
AU  - Beguinot F
LA  - eng
PT  - Journal Article
PT  - Expression of Concern
DEP - 20171106
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
ECF - Diabetes. 2000 Jul;49(7):1194-202. PMID: 10909978
PMC - PMC5780054
EDAT- 2017/11/08 06:00
MHDA- 2017/11/08 06:00
CRDT- 2017/11/08 06:00
PMCR- 2019/02/01 00:00
PHST- 2019/02/01 00:00 [pmc-release]
PHST- 2017/11/08 06:00 [entrez]
PHST- 2017/11/08 06:00 [pubmed]
PHST- 2017/11/08 06:00 [medline]
AID - db17-ec2017a [pii]
AID - 10.2337/db17-ec2017a [doi]
PST - aheadofprint
SO  - Diabetes. 2017 Nov 6. pii: db17-ec2017a. doi: 10.2337/db17-ec2017a.

PMID- 29122892
OWN - NLM
STAT- MEDLINE
DCOM- 20180508
LR  - 20180519
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 41
IP  - 1
DP  - 2018 Jan
TI  - Subclinical First Trimester Renal Abnormalities Are Associated With Preeclampsia 
      in Normoalbuminuric Women With Type 1 Diabetes.
PG  - 120-127
LID - 10.2337/dc17-1635 [doi]
AB  - OBJECTIVE: This study was conducted to determine the utility of tubular
      (urinary/plasma neutrophil gelatinase-associated lipocalin [NGAL] and urinary
      kidney injury molecule 1 [KIM-1]) and glomerular (estimated glomerular filtration
      rate [eGFR]) biomarkers in predicting preeclampsia (PE) in pregnant women with
      type 1 diabetes mellitus (T1DM) who were free of microalbuminuria and
      hypertension at the first trimester. RESEARCH DESIGN AND METHODS: This was a
      prospective study of T1DM pregnancy. Maternal urinary and plasma NGAL, urinary
      KIM-1 (ELISA of frozen samples), and eGFR (Chronic Kidney Disease Epidemiology
      Collaboration equation) were determined at three study visits (V1: 12.4 +/- 1.8; 
      V2: 21.7 +/- 1.4; V3: 31.4 +/- 1.5 weeks' gestation [mean +/- SD]) in 23 women
      with T1DM with subsequent PE (DM+PE+), 24 who remained normotensive (DM+PE-),
      and, for reference, in 19 normotensive pregnant women without diabetes (DM-). The
      groups with diabetes were matched for age, diabetes duration, and parity. All
      subjects were normotensive and free of microalbuminuria or albuminuria at V1. All
      study visits preceded the onset of PE. RESULTS: Urinary creatinine-corrected NGAL
      (uNGALcc, ng/mg) was significantly elevated at V1 in DM+PE+ vs. DM+PE- women (P =
      0.01); this remained significant after exclusion of leukocyte-positive samples (5
      DM+PE+ and 2 DM+PE-) (P = 0.02). Accounting for BMI, HbA1c, and total daily
      insulin dose, a doubling of uNGALcc at V1 conferred a sevenfold increase in risk 
      for PE (P = 0.026). In contrast, neither plasma NGAL nor urinary KIM-1 predicted 
      PE. Also at V1, eGFR was elevated in DM+PE+ vs. DM+PE- (P = 0.04). CONCLUSIONS:
      Early tubular and glomerular dysfunction may predict PE in first trimester women 
      with T1DM, even if free of microalbuminuria. These data suggest that subclinical 
      renal tubular and glomerular injury, if present early in pregnancy, may
      predispose women with T1DM to PE.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Kelly, Clare B
AU  - Kelly CB
AD  - Centre for Experimental Medicine, Queen's University Belfast, Belfast, Northern
      Ireland, U.K.
AD  - Division of Endocrinology, Medical University of South Carolina, Charleston, SC.
FAU - Hookham, Michelle B
AU  - Hookham MB
AD  - Centre for Experimental Medicine, Queen's University Belfast, Belfast, Northern
      Ireland, U.K.
AD  - The Department of Clinical Biochemistry, Royal Victoria Hospital, Belfast,
      Northern Ireland, U.K.
FAU - Yu, Jeremy Y
AU  - Yu JY
AD  - Centre for Experimental Medicine, Queen's University Belfast, Belfast, Northern
      Ireland, U.K.
AD  - Division of Endocrinology, Medical University of South Carolina, Charleston, SC.
FAU - Jenkins, Alicia J
AU  - Jenkins AJ
AD  - Division of Endocrinology, Medical University of South Carolina, Charleston, SC.
AD  - National Health and Medical Research Council Clinical Trials Centre, University
      of Sydney, Camperdown, Sydney, New South Wales, Australia.
FAU - Nankervis, Alison J
AU  - Nankervis AJ
AD  - Diabetes Service, The Royal Women's Hospital, Melbourne, Victoria, Australia.
FAU - Hanssen, Kristian F
AU  - Hanssen KF
AD  - Department of Endocrinology, Oslo University Hospital, Oslo, Norway.
AD  - Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
FAU - Garg, Satish K
AU  - Garg SK
AD  - Barbara Davis Center for Childhood Diabetes, University of Colorado, Denver, CO.
FAU - Scardo, James A
AU  - Scardo JA
AD  - Spartanburg Regional Medical Center, Spartanburg, SC.
FAU - Hammad, Samar M
AU  - Hammad SM
AD  - Department of Regenerative Medicine and Cell Biology, Medical University of South
      Carolina, Charleston, SC.
FAU - Menard, M Kathryn
AU  - Menard MK
AD  - Division of Materno-Fetal Medicine, University of North Carolina, Chapel Hill,
      NC.
FAU - Aston, Christopher E
AU  - Aston CE
AD  - Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma
      City, OK.
FAU - Lyons, Timothy J
AU  - Lyons TJ
AUID- ORCID: 0000-0003-2106-1622
AD  - Centre for Experimental Medicine, Queen's University Belfast, Belfast, Northern
      Ireland, U.K. lyonstj@musc.edu.
AD  - Division of Endocrinology, Medical University of South Carolina, Charleston, SC.
LA  - eng
GR  - M01 RR001070/RR/NCRR NIH HHS/United States
GR  - M01 RR014467/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20171109
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (Biomarkers)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (HAVCR1 protein, human)
RN  - 0 (Hepatitis A Virus Cellular Receptor 1)
RN  - 0 (LCN2 protein, human)
RN  - 0 (Lipocalin-2)
RN  - AYI8EX34EU (Creatinine)
SB  - IM
CIN - Diabetes Care. 2018 Jun;41(6):e101. PMID: 29784705
CIN - Diabetes Care. 2018 Jun;41(6):e102-e103. PMID: 29784706
MH  - Adult
MH  - Albuminuria/blood/*urine
MH  - Biomarkers/blood/urine
MH  - Body Mass Index
MH  - Creatinine/blood/urine
MH  - Diabetes Mellitus, Type 1/blood/*urine
MH  - Female
MH  - Glomerular Filtration Rate
MH  - Glycated Hemoglobin A/metabolism
MH  - Hepatitis A Virus Cellular Receptor 1/metabolism
MH  - Humans
MH  - Kidney Diseases/blood/*urine
MH  - Lipocalin-2/blood/urine
MH  - Pre-Eclampsia/blood/*urine
MH  - Pregnancy
MH  - Pregnancy Trimester, First/blood/*urine
MH  - Pregnancy in Diabetics/blood/*urine
MH  - Prospective Studies
MH  - Young Adult
PMC - PMC5741157
EDAT- 2017/11/11 06:00
MHDA- 2018/05/09 06:00
CRDT- 2017/11/11 06:00
PMCR- 2019/01/01 00:00
PHST- 2017/08/04 00:00 [received]
PHST- 2017/10/05 00:00 [accepted]
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/11/11 06:00 [pubmed]
PHST- 2018/05/09 06:00 [medline]
PHST- 2017/11/11 06:00 [entrez]
AID - dc17-1635 [pii]
AID - 10.2337/dc17-1635 [doi]
PST - ppublish
SO  - Diabetes Care. 2018 Jan;41(1):120-127. doi: 10.2337/dc17-1635. Epub 2017 Nov 9.

PMID- 29118060
OWN - NLM
STAT- MEDLINE
DCOM- 20180508
LR  - 20180519
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 41
IP  - 1
DP  - 2018 Jan
TI  - Association Between Inflammatory Markers and Progression to Kidney Dysfunction:
      Examining Different Assessment Windows in Patients With Type 1 Diabetes.
PG  - 128-135
LID - 10.2337/dc17-0867 [doi]
AB  - OBJECTIVE: To determine whether biomarkers of inflammation and endothelial
      dysfunction are associated with the development of kidney dysfunction and the
      time frame of their association. RESEARCH DESIGN AND METHODS: Biomarkers were
      measured at four time points during 28 years of treatment and follow-up in
      patients with type 1 diabetes in the Diabetes Control and Complications
      Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC)
      cohort. In addition to traditional biomarkers of inflammation (C-reactive protein
      and fibrinogen), we measured interleukin-6 (IL-6) and soluble tumor necrosis
      factor receptors 1 and 2 (sTNFR-1/2), markers of endothelial dysfunction (soluble
      intracellular adhesion molecule-1, vascular cell adhesion molecule-1, and
      E-selectin [sE-selectin]), and fibrinolysis (total and active plasminogen
      activator inhibitor-1 [PAI-1]). Renal outcomes were defined as progression to
      incident chronic kidney disease (stage 3 or more severe) or macroalbuminuria
      (albumin excretion rate >/=300 mg/24 h). Prospective multivariate event-time
      analyses were used to determine the association of each biomarker with each
      subsequent event within prespecified intervals (3-year and 10-year windows).
      RESULTS: Multivariate event-time models indicated that several markers of
      inflammation (sTNFR-1/2), endothelial dysfunction (sE-selectin), and
      clotting/fibrinolysis (fibrinogen and PAI-1) are significantly associated with
      subsequent development of kidney dysfunction. Although some markers showed
      variations in the associations between the follow-up windows examined, the
      results indicate that biomarkers (sTNFR-1/2, sE-selectin, PAI-1, and fibrinogen) 
      are associated with progression to chronic kidney disease in both the 3-year and 
      the 10-year windows. CONCLUSIONS: Plasma markers of inflammation, endothelial
      dysfunction, and clotting/fibrinolysis are associated with progression to kidney 
      dysfunction in type 1 diabetes during both short-term and long-term follow-up.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Baker, Nathaniel L
AU  - Baker NL
AUID- ORCID: 0000-0003-3313-1579
AD  - Department of Public Health Sciences, Medical University of South Carolina,
      Charleston, SC bakern@musc.edu.
FAU - Hunt, Kelly J
AU  - Hunt KJ
AUID- ORCID: 0000-0001-8999-3587
AD  - Department of Public Health Sciences, Medical University of South Carolina,
      Charleston, SC.
AD  - Ralph H. Johnson VA Medical Center, Charleston, SC.
FAU - Stevens, Danielle R
AU  - Stevens DR
AD  - Department of Public Health Sciences, Medical University of South Carolina,
      Charleston, SC.
FAU - Jarai, Gabor
AU  - Jarai G
AD  - Discovery Biology, Fibrotic Diseases, Bristol-Myers Squibb, Pennington, NJ.
FAU - Rosen, Glenn D
AU  - Rosen GD
AD  - Translational Research and Discovery, Fibrotic Diseases, Bristol-Myers Squibb,
      Pennington, NJ.
FAU - Klein, Richard L
AU  - Klein RL
AD  - Ralph H. Johnson VA Medical Center, Charleston, SC.
FAU - Virella, Gabriel
AU  - Virella G
AD  - Department of Microbiology and Immunology, Medical University of South Carolina, 
      Charleston, SC.
FAU - Lopes-Virella, Maria F
AU  - Lopes-Virella MF
AD  - Ralph H. Johnson VA Medical Center, Charleston, SC.
AD  - Department of Medicine and Laboratory Services, Medical University of South
      Carolina, Charleston, SC.
CN  - DCCT/EDIC Research Group
LA  - eng
GR  - R01 DK081352/DK/NIDDK NIH HHS/United States
GR  - R01 DK099177/DK/NIDDK NIH HHS/United States
GR  - TL1 TR001451/TR/NCATS NIH HHS/United States
GR  - UL1 TR001450/TR/NCATS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20171108
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (Biomarkers)
RN  - 0 (E-Selectin)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (ICAM1 protein, human)
RN  - 0 (IL6 protein, human)
RN  - 0 (Interleukin-6)
RN  - 0 (Plasminogen Activator Inhibitor 1)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (SELE protein, human)
RN  - 0 (SERPINE1 protein, human)
RN  - 0 (TNFRSF1A protein, human)
RN  - 0 (Triglycerides)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 9001-32-5 (Fibrinogen)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - 97C5T2UQ7J (Cholesterol)
SB  - IM
MH  - Adult
MH  - Biomarkers/*blood
MH  - Blood Coagulation
MH  - C-Reactive Protein/metabolism
MH  - Cholesterol/blood
MH  - Cross-Sectional Studies
MH  - Diabetes Complications/*blood/*diagnosis
MH  - Diabetes Mellitus, Type 1/*blood
MH  - *Disease Progression
MH  - E-Selectin/blood
MH  - Female
MH  - Fibrinogen/metabolism
MH  - Fibrinolysis
MH  - Follow-Up Studies
MH  - Glycated Hemoglobin A/metabolism
MH  - Humans
MH  - Inflammation/blood
MH  - Intercellular Adhesion Molecule-1/blood
MH  - Interleukin-6/blood
MH  - Kidney Diseases/*blood/diagnosis
MH  - Male
MH  - Middle Aged
MH  - Plasminogen Activator Inhibitor 1/blood
MH  - Prospective Studies
MH  - Receptors, Tumor Necrosis Factor, Type I/blood
MH  - Receptors, Tumor Necrosis Factor, Type II/blood
MH  - Triglycerides/blood
MH  - Vascular Cell Adhesion Molecule-1/blood
MH  - Young Adult
PMC - PMC5741153
EDAT- 2017/11/10 06:00
MHDA- 2018/05/09 06:00
CRDT- 2017/11/10 06:00
PMCR- 2019/01/01 00:00
PHST- 2017/05/03 00:00 [received]
PHST- 2017/10/05 00:00 [accepted]
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/11/10 06:00 [pubmed]
PHST- 2018/05/09 06:00 [medline]
PHST- 2017/11/10 06:00 [entrez]
AID - dc17-0867 [pii]
AID - 10.2337/dc17-0867 [doi]
PST - ppublish
SO  - Diabetes Care. 2018 Jan;41(1):128-135. doi: 10.2337/dc17-0867. Epub 2017 Nov 8.

PMID- 29118059
OWN - NLM
STAT- MEDLINE
DCOM- 20180515
LR  - 20180519
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 41
IP  - 1
DP  - 2018 Jan
TI  - Diabetes Care Disparities in Long-standing Type 1 Diabetes in Canada and the
      U.S.: A Cross-sectional Comparison.
PG  - 88-95
LID - 10.2337/dc17-1074 [doi]
AB  - OBJECTIVE: To assess national differences in diabetes care and quality of life
      (QOL) between individuals with long-standing type 1 diabetes (>/=50 years) in
      Canada and the U.S. RESEARCH DESIGN AND METHODS: Cross-sectional data from
      identical surveys administered in the Canadian Study of Longevity in Diabetes and
      the Joslin Medalist Study, collected in 2013-2016 and 2005-2011, respectively,
      were compared. Laboratory values and ophthalmic examination were completed by
      clinical care physicians for Canadians and the Joslin Clinic for Americans.
      Univariate comparisons and multivariable regression for HbA1c, QOL, insulin pump 
      use, and coronary artery disease (CAD) were performed. Nephropathy, CAD, and
      peripheral arterial disease (PAD) were self-reported; neuropathy was defined by a
      Michigan Neuropathy Screening Instrument (Questionnaire component) score >/=3,
      and proliferative retinopathy was documented from ophthalmic examination. QOL was
      self-reported on an ordinal scale. RESULTS: Three hundred sixty-one Canadians and
      668 Americans had similar ages (mean 65.78 years [SD 8.67] vs. 66.38 years
      [7.66], P = 0.27) and durations of diabetes (median 53.00 years [interquartile
      range 51.00, 58.00] vs. 53.00 years [51.00, 57.00], P = 0.51). Canadians had
      higher HbA1c (mean 7.53% [SD 1.03] [59 mmol/mol] vs. 7.22% [0.98] [55 mmol/mol], 
      P < 0.0001), lower QOL (36.9% vs. 48.7% with "excellent" QOL, P = 0.0002), and
      less CAD (29.7% vs. 41.2%, P = 0.0003) and insulin pump use (43.3% vs. 55.6%, P =
      0.0002). Other complication rates were similar. Residual differences for
      Canadians compared with Americans remained after adjustment for age, sex, CAD,
      PAD, education, and relevant a priori selected variables: 0.28% higher HbA1c (P =
      0.0004); and odds ratios of 0.68 (95% CI 0.51, 0.90), 0.46 (0.31, 0.68), and 0.71
      (0.52, 0.96) for higher QOL, CAD, and insulin pump use, respectively.
      CONCLUSIONS: Although Canadians and Americans have similar rates of complications
      other than CAD, further research is required to understand why Canadians have
      higher HbA1c levels, lower QOL, and less insulin pump use.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Weisman, Alanna
AU  - Weisman A
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario,
      Canada.
AD  - Division of Endocrinology and Metabolism, Department of Medicine, University of
      Toronto, Toronto, Ontario, Canada.
FAU - Lovblom, Leif E
AU  - Lovblom LE
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario,
      Canada.
FAU - Keenan, Hillary A
AU  - Keenan HA
AUID- ORCID: 0000-0003-4172-5537
AD  - Research Division, Joslin Diabetes Center, Boston, MA.
FAU - Tinsley, Liane J
AU  - Tinsley LJ
AD  - Research Division, Joslin Diabetes Center, Boston, MA.
FAU - D'Eon, Stephanie
AU  - D'Eon S
AD  - Research Division, Joslin Diabetes Center, Boston, MA.
FAU - Boulet, Genevieve
AU  - Boulet G
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario,
      Canada.
FAU - Farooqi, Mohammed A
AU  - Farooqi MA
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario,
      Canada.
FAU - Lovshin, Julie A
AU  - Lovshin JA
AUID- ORCID: 0000-0002-9171-8952
AD  - Division of Endocrinology and Metabolism, Department of Medicine, University of
      Toronto, Toronto, Ontario, Canada.
AD  - Department of Physiology, University of Toronto, Toronto, Ontario, Canada.
FAU - Orszag, Andrej
AU  - Orszag A
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario,
      Canada.
FAU - Lytvyn, Yuliya
AU  - Lytvyn Y
AD  - Department of Physiology, University of Toronto, Toronto, Ontario, Canada.
AD  - Division of Nephrology, Department of Medicine, University of Toronto, Toronto,
      Ontario, Canada.
FAU - Brent, Michael H
AU  - Brent MH
AD  - Department of Ophthalmology & Vision Sciences and Department of Medicine,
      University of Toronto, Toronto, Ontario, Canada.
FAU - Paul, Narinder
AU  - Paul N
AD  - Division of Cardiothoracic Imaging, Joint Department of Medical Imaging,
      University Health Network, Toronto, Ontario, Canada.
FAU - Bril, Vera
AU  - Bril V
AUID- ORCID: 0000-0002-5805-4883
AD  - Division of Neurology, Department of Medicine, University of Toronto, Toronto,
      Ontario, Canada.
FAU - Cherney, David Z
AU  - Cherney DZ
AUID- ORCID: 0000-0003-4164-0429
AD  - Department of Physiology, University of Toronto, Toronto, Ontario, Canada.
AD  - Division of Nephrology, Department of Medicine, University of Toronto, Toronto,
      Ontario, Canada.
FAU - Perkins, Bruce A
AU  - Perkins BA
AUID- ORCID: 0000-0002-5885-0046
AD  - Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario,
      Canada bruce.perkins@sinaihealthsystem.ca.
AD  - Division of Endocrinology and Metabolism, Department of Medicine, University of
      Toronto, Toronto, Ontario, Canada.
LA  - eng
GR  - DP3 DK094333/DK/NIDDK NIH HHS/United States
GR  - P30 DK036836/DK/NIDDK NIH HHS/United States
GR  - R24 DK083957/DK/NIDDK NIH HHS/United States
GR  - UL1 RR025758/RR/NCRR NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20171108
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (Insulin)
SB  - IM
MH  - Aged
MH  - Body Mass Index
MH  - Canada/epidemiology
MH  - Coronary Artery Disease/*epidemiology/prevention & control
MH  - Cross-Sectional Studies
MH  - Diabetes Mellitus, Type 1/complications/drug therapy/*epidemiology
MH  - Diabetic Retinopathy/*epidemiology/prevention & control
MH  - Dose-Response Relationship, Drug
MH  - Female
MH  - Glycated Hemoglobin A/metabolism
MH  - *Healthcare Disparities
MH  - Humans
MH  - Insulin/therapeutic use
MH  - Insulin Infusion Systems
MH  - Longevity
MH  - Male
MH  - Middle Aged
MH  - Peripheral Arterial Disease/*epidemiology/prevention & control
MH  - Prevalence
MH  - Quality of Life
MH  - Surveys and Questionnaires
MH  - United States/epidemiology
PMC - PMC5741151
EDAT- 2017/11/10 06:00
MHDA- 2018/05/16 06:00
CRDT- 2017/11/10 06:00
PMCR- 2019/01/01 00:00
PHST- 2017/05/29 00:00 [received]
PHST- 2017/10/05 00:00 [accepted]
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/11/10 06:00 [pubmed]
PHST- 2018/05/16 06:00 [medline]
PHST- 2017/11/10 06:00 [entrez]
AID - dc17-1074 [pii]
AID - 10.2337/dc17-1074 [doi]
PST - ppublish
SO  - Diabetes Care. 2018 Jan;41(1):88-95. doi: 10.2337/dc17-1074. Epub 2017 Nov 8.

PMID- 29113984
OWN - NLM
STAT- MEDLINE
DCOM- 20180508
LR  - 20180519
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 41
IP  - 1
DP  - 2018 Jan
TI  - Cardiovascular Complications Over 5 Years and Their Association With Survival in 
      the GERODIAB Cohort of Elderly French Patients With Type 2 Diabetes.
PG  - 156-162
LID - 10.2337/dc17-1437 [doi]
AB  - OBJECTIVE: The GERODIAB study is a multicenter prospective observational study
      performed over 5 years in French patients aged 70 years or above with type 2
      diabetes. This report deals with their cardiovascular complications and their
      relationship with survival. RESEARCH DESIGN AND METHODS: Consecutive patients (n 
      = 987, median age = 77 years) were included from 56 diabetes centers over 1 year.
      Individual characteristics, history and complications of diabetes, geriatric
      factors, and clinical and biological parameters were recorded. Survival was
      analyzed using the Kaplan-Meier method and proportional hazards regression
      models. RESULTS: The frequency of cardiovascular complications increased from 47%
      at inclusion to 67% at 5 years. The most frequent complications were coronary
      heart disease (increasing from 30% to 41%) and vascular disease of the lower
      limbs (25% to 35%) and of the cerebral vessels (15% to 26%). Heart failure was
      less common, but its frequency doubled during the follow-up (9% to 20%). It was
      strongly associated with poor survival (P < 0.0001), as was vascular disease of
      the lower limbs (P = 0.0004), whereas coronary heart disease (P = 0.0056) and
      vascular disease of cerebral vessels (P = 0.026) had mild associations.
      Amputation (P < 0.0001) and foot wounds (P < 0.0001) were strongly associated
      with survival. In multivariate models, heart failure was the strongest predictor 
      of poor survival (hazard ratio [HR] 1.96 [95% CI 1.45-2.64]; P < 0.0001). It
      remained significant when other factors were considered simultaneously (HR 1.92
      [95% CI 1.43-2.58]; P < 0.0001). CONCLUSIONS: Cardiovascular complications are
      associated with poor survival in elderly patients with type 2 diabetes,
      especially heart failure.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Bauduceau, Bernard
AU  - Bauduceau B
AD  - Endocrinology, Begin Hospital, Saint Mande, France.
FAU - Le Floch, Jean-Pierre
AU  - Le Floch JP
AUID- ORCID: 0000-0003-1957-3477
AD  - Diabetology-Endocrinology, Villecresnes Medical Hospital, Villecresnes, France
      jplefloch@dietvill.com.
FAU - Halimi, Serge
AU  - Halimi S
AD  - Diabetology, Endocrinology, Grenoble Alpes University, Grenoble, France.
FAU - Verny, Christiane
AU  - Verny C
AD  - Gerontology, Bicetre University Hospital, Le Kremlin-Bicetre, France.
FAU - Doucet, Jean
AU  - Doucet J
AD  - Internal Medicine, Geriatrics and Therapeutics, Saint Julien Hospital, Rouen
      University Hospital, Rouen, France.
CN  - SFD/SFGG Intergroup
LA  - eng
SI  - ClinicalTrials.gov/NCT01282060
PT  - Journal Article
PT  - Multicenter Study
PT  - Observational Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20171107
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
RN  - 0 (Hypoglycemic Agents)
RN  - 9100L32L2N (Metformin)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Blood Pressure
MH  - Cardiovascular Diseases/*blood/complications/drug therapy
MH  - Diabetes Complications/*blood/complications/drug therapy
MH  - Diabetes Mellitus, Type 2/*blood/complications/drug therapy
MH  - Female
MH  - Follow-Up Studies
MH  - Glycated Hemoglobin A/metabolism
MH  - Humans
MH  - Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use
MH  - Hypoglycemic Agents/therapeutic use
MH  - Male
MH  - Metformin/therapeutic use
MH  - Proportional Hazards Models
MH  - Prospective Studies
MH  - Risk Factors
EDAT- 2017/11/09 06:00
MHDA- 2018/05/09 06:00
CRDT- 2017/11/09 06:00
PHST- 2017/07/17 00:00 [received]
PHST- 2017/10/04 00:00 [accepted]
PHST- 2017/11/09 06:00 [pubmed]
PHST- 2018/05/09 06:00 [medline]
PHST- 2017/11/09 06:00 [entrez]
AID - dc17-1437 [pii]
AID - 10.2337/dc17-1437 [doi]
PST - ppublish
SO  - Diabetes Care. 2018 Jan;41(1):156-162. doi: 10.2337/dc17-1437. Epub 2017 Nov 7.

PMID- 29113983
OWN - NLM
STAT- MEDLINE
DCOM- 20180508
LR  - 20180519
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 41
IP  - 1
DP  - 2018 Jan
TI  - FGF23 Concentration and APOL1 Genotype Are Novel Predictors of Mortality in
      African Americans With Type 2 Diabetes.
PG  - 178-186
LID - 10.2337/dc17-0820 [doi]
AB  - OBJECTIVE: Cardiovascular and renal complications contribute to higher mortality 
      in patients with diabetes. We assessed novel and conventional predictors of
      mortality in African American-Diabetes Heart Study (AA-DHS) participants.
      RESEARCH DESIGN AND METHODS: Associations between mortality and subclinical
      atherosclerosis, urine albumin-to-creatinine ratio (UACR), estimated glomerular
      filtration rate (eGFR), plasma fibroblast growth factor 23 (FGF23) concentration,
      African ancestry proportion, and apolipoprotein L1 genotypes (APOL1) were
      assessed in 513 African Americans with type 2 diabetes; analyses were performed
      using Cox proportional hazards models. RESULTS: At baseline, participants were
      55.6% female with median (25th, 75th percentile) age 55 years (49.0, 62.0),
      diabetes duration 8 years (5.0, 13.0), glycosylated hemoglobin 60.7 mmol/mol
      (48.6, 76.0), eGFR 91.3 mL/min/1.73 m(2) (76.4, 111.3), UACR 12.5 mg/mmol (4.2,
      51.2), and coronary artery calcium 28.5 mg Ca(2+) (1.0, 348.6); 11.5% had two
      APOL1 renal-risk variants. After 6.6-year follow-up (5.8, 7.5), 54 deaths were
      recorded. Higher levels of coronary artery calcified plaque, carotid artery
      calcified plaque, albuminuria, and FGF23 were associated with higher mortality
      after adjustment for age, sex, and African ancestry proportion. A penalized Cox
      regression that included all covariates and predictors associated with mortality 
      identified male sex (hazard ratio [HR] 4.17 [95% CI 1.96-9.09]), higher FGF23 (HR
      2.10 [95% CI 1.59-2.78]), and absence of APOL1 renal-risk genotypes (HR 0.07 [95%
      CI 0.01-0.69]) as the strongest predictors of mortality. CONCLUSIONS: Accounting 
      for conventional risk factors, higher FGF23 concentrations and APOL1
      non-renal-risk genotypes associated with higher mortality in African Americans
      with diabetes. These data add to growing evidence supporting FGF23 association
      with mortality; mechanisms whereby these novel predictors impact survival remain 
      to be determined.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Chan, Gary C
AU  - Chan GC
AD  - Section on Nephrology, Department of Internal Medicine, Wake Forest School of
      Medicine, Winston-Salem, NC.
AD  - Division of Nephrology, Department of Medicine, University of Hong Kong, Hong
      Kong, China.
FAU - Divers, Jasmin
AU  - Divers J
AD  - Department of Biostatistical Sciences, Division of Public Health Sciences, Wake
      Forest School of Medicine, Winston-Salem, NC.
FAU - Russell, Gregory B
AU  - Russell GB
AD  - Department of Biostatistical Sciences, Division of Public Health Sciences, Wake
      Forest School of Medicine, Winston-Salem, NC.
FAU - Langefeld, Carl D
AU  - Langefeld CD
AD  - Department of Biostatistical Sciences, Division of Public Health Sciences, Wake
      Forest School of Medicine, Winston-Salem, NC.
FAU - Wagenknecht, Lynne E
AU  - Wagenknecht LE
AD  - Department of Biostatistical Sciences, Division of Public Health Sciences, Wake
      Forest School of Medicine, Winston-Salem, NC.
FAU - Hsu, Fang-Chi
AU  - Hsu FC
AD  - Department of Biostatistical Sciences, Division of Public Health Sciences, Wake
      Forest School of Medicine, Winston-Salem, NC.
FAU - Xu, Jianzhao
AU  - Xu J
AD  - Department of Biochemistry, Center for Genomics and Personalized Medicine
      Research, and Center for Diabetes Research, Wake Forest School of Medicine,
      Winston-Salem, NC.
FAU - Smith, S Carrie
AU  - Smith SC
AD  - Department of Biochemistry, Center for Genomics and Personalized Medicine
      Research, and Center for Diabetes Research, Wake Forest School of Medicine,
      Winston-Salem, NC.
FAU - Palmer, Nicholette D
AU  - Palmer ND
AUID- ORCID: 0000-0001-8883-2511
AD  - Department of Biochemistry, Center for Genomics and Personalized Medicine
      Research, and Center for Diabetes Research, Wake Forest School of Medicine,
      Winston-Salem, NC.
FAU - Hicks, Pamela J
AU  - Hicks PJ
AD  - Department of Biochemistry, Center for Genomics and Personalized Medicine
      Research, and Center for Diabetes Research, Wake Forest School of Medicine,
      Winston-Salem, NC.
FAU - Bowden, Donald W
AU  - Bowden DW
AD  - Department of Biochemistry, Center for Genomics and Personalized Medicine
      Research, and Center for Diabetes Research, Wake Forest School of Medicine,
      Winston-Salem, NC.
FAU - Register, Thomas C
AU  - Register TC
AD  - Department of Pathology, Wake Forest School of Medicine, Winston-Salem, NC.
FAU - Ma, Lijun
AU  - Ma L
AD  - Section on Nephrology, Department of Internal Medicine, Wake Forest School of
      Medicine, Winston-Salem, NC.
FAU - Carr, J Jeffrey
AU  - Carr JJ
AD  - Department of Radiology, Vanderbilt University School of Medicine, Nashville, TN.
FAU - Freedman, Barry I
AU  - Freedman BI
AUID- ORCID: 0000-0003-0275-5530
AD  - Section on Nephrology, Department of Internal Medicine, Wake Forest School of
      Medicine, Winston-Salem, NC bfreedma@wakehealth.edu.
LA  - eng
GR  - R01 AR048797/AR/NIAMS NIH HHS/United States
GR  - R01 DK071891/DK/NIDDK NIH HHS/United States
GR  - R01 HL067348/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20171107
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (APOL1 protein, human)
RN  - 0 (Apolipoprotein L1)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (fibroblast growth factor 23)
RN  - 62031-54-3 (Fibroblast Growth Factors)
RN  - AYI8EX34EU (Creatinine)
SB  - IM
CIN - Diabetes Care. 2018 May;41(5):e78. PMID: 29678869
CIN - Diabetes Care. 2018 May;41(5):e79-e80. PMID: 29678870
MH  - African Americans/*genetics
MH  - Albuminuria/genetics/mortality
MH  - Apolipoprotein L1/blood/*genetics
MH  - Atherosclerosis/genetics/mortality
MH  - Cohort Studies
MH  - Creatinine
MH  - Diabetes Mellitus, Type 2/*genetics/*mortality
MH  - Female
MH  - Fibroblast Growth Factors/blood/*genetics
MH  - Follow-Up Studies
MH  - Genotyping Techniques
MH  - Glomerular Filtration Rate
MH  - Glycated Hemoglobin A/metabolism
MH  - Humans
MH  - Kidney Function Tests
MH  - Male
MH  - Middle Aged
MH  - Proportional Hazards Models
MH  - Risk Factors
PMC - PMC5741152
EDAT- 2017/11/09 06:00
MHDA- 2018/05/09 06:00
CRDT- 2017/11/09 06:00
PMCR- 2019/01/01 00:00
PHST- 2017/04/24 00:00 [received]
PHST- 2017/10/05 00:00 [accepted]
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/11/09 06:00 [pubmed]
PHST- 2018/05/09 06:00 [medline]
PHST- 2017/11/09 06:00 [entrez]
AID - dc17-0820 [pii]
AID - 10.2337/dc17-0820 [doi]
PST - ppublish
SO  - Diabetes Care. 2018 Jan;41(1):178-186. doi: 10.2337/dc17-0820. Epub 2017 Nov 7.

PMID- 29109299
OWN - NLM
STAT- MEDLINE
DCOM- 20180515
LR  - 20180519
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 41
IP  - 1
DP  - 2018 Jan
TI  - Long-term Trends in Antidiabetes Drug Usage in the U.S.: Real-world Evidence in
      Patients Newly Diagnosed With Type 2 Diabetes.
PG  - 69-78
LID - 10.2337/dc17-1414 [doi]
AB  - OJBECTIVE: To explore temporal trends in antidiabetes drug (ADD) prescribing and 
      intensification patterns, along with glycemic levels and comorbidities, and
      possible benefits of novel ADDs in delaying the need for insulin initiation in
      patients diagnosed with type 2 diabetes. RESEARCH DESIGN AND METHODS: Patients
      with type 2 diabetes aged 18-80 years, who initiated any ADD, were selected (n = 
      1,023,340) from the U.S. Centricity Electronic Medical Records. Those who
      initiated second-line ADD after first-line metformin were identified (subcohort
      1, n = 357,482); the third-line therapy choices were further explored. RESULTS:
      From 2005 to 2016, first-line use increased for metformin (60-77%) and decreased 
      for sulfonylureas (20-8%). During a mean follow-up of 3.4 years post metformin,
      48% initiated a second ADD at a mean HbA1c of 8.4%. In subcohort 1, although
      sulfonylurea usage as second-line treatment decreased (60-46%), it remained the
      most popular second ADD choice. Use increased for insulin (7-17%) and dipeptidyl 
      peptidase-4 inhibitors (DPP-4i) (0.4-21%). The rates of intensification with
      insulin and sulfonylureas did not decline over the last 10 years. The restricted 
      mean time to insulin initiation was marginally longer in second-line DPP-4i (7.1 
      years) and in the glucagon-like peptide 1 receptor agonist group (6.6 years)
      compared with sulfonylurea (6.3 years, P < 0.05). CONCLUSIONS: Most patients
      initiate second-line therapy at elevated HbA1c levels, with highly heterogeneous 
      clinical characteristics across ADD classes. Despite the introduction of newer
      therapies, sulfonylureas remained the most popular second-line agent, and the
      rates of intensification with sulfonylureas and insulin remained consistent over 
      time. The incretin-based therapies were associated with a small delay in the need
      for therapy intensification compared with sulfonylureas.
CI  - (c) 2017 by the American Diabetes Association.
FAU - Montvida, Olga
AU  - Montvida O
AD  - Statistics Unit, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
AD  - Faculty of Health, School of Biomedical Sciences, Queensland University of
      Technology, Brisbane, Australia.
FAU - Shaw, Jonathan
AU  - Shaw J
AD  - Baker Heart and Diabetes Institute, Melbourne, Australia.
FAU - Atherton, John J
AU  - Atherton JJ
AD  - Cardiology Department, Royal Brisbane and Women's Hospital, and University of
      Queensland School of Medicine, Brisbane, Australia.
FAU - Stringer, Frances
AU  - Stringer F
AD  - Model Answers Pty Ltd, Brisbane, Australia.
FAU - Paul, Sanjoy K
AU  - Paul SK
AUID- ORCID: 0000-0003-0848-7194
AD  - Statistics Unit, QIMR Berghofer Medical Research Institute, Brisbane, Australia
      sanjoy.paul@unimelb.edu.au.
AD  - Melbourne EpiCentre, University of Melbourne, Melbourne, Australia.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171106
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (Blood Glucose)
RN  - 0 (Dipeptidyl-Peptidase IV Inhibitors)
RN  - 0 (Glucagon-Like Peptide-1 Receptor)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Incretins)
RN  - 0 (Insulin)
RN  - 0 (Sulfonylurea Compounds)
RN  - 9100L32L2N (Metformin)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Blood Glucose/analysis
MH  - Diabetes Mellitus, Type 2/diagnosis/*drug therapy
MH  - Dipeptidyl-Peptidase IV Inhibitors/therapeutic use
MH  - Female
MH  - Follow-Up Studies
MH  - Glucagon-Like Peptide-1 Receptor/agonists/metabolism
MH  - Humans
MH  - Hypoglycemic Agents/*therapeutic use
MH  - Incretins/therapeutic use
MH  - Insulin/therapeutic use
MH  - Longitudinal Studies
MH  - Male
MH  - Metformin/therapeutic use
MH  - Middle Aged
MH  - Sulfonylurea Compounds/therapeutic use
MH  - Time Factors
MH  - Young Adult
EDAT- 2017/11/08 06:00
MHDA- 2018/05/16 06:00
CRDT- 2017/11/08 06:00
PHST- 2017/07/14 00:00 [received]
PHST- 2017/09/25 00:00 [accepted]
PHST- 2017/11/08 06:00 [pubmed]
PHST- 2018/05/16 06:00 [medline]
PHST- 2017/11/08 06:00 [entrez]
AID - dc17-1414 [pii]
AID - 10.2337/dc17-1414 [doi]
PST - ppublish
SO  - Diabetes Care. 2018 Jan;41(1):69-78. doi: 10.2337/dc17-1414. Epub 2017 Nov 6.

PMID- 29109298
OWN - NLM
STAT- MEDLINE
DCOM- 20180515
LR  - 20180519
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 41
IP  - 1
DP  - 2018 Jan
TI  - Severity of Neuropathy Is Associated With Long-term Spinal Cord Stimulation
      Outcome in Painful Diabetic Peripheral Neuropathy: Five-Year Follow-up of a
      Prospective Two-Center Clinical Trial.
PG  - 32-38
LID - 10.2337/dc17-0983 [doi]
AB  - OBJECTIVE: Evidence from prospective studies for long-term treatment efficacy of 
      spinal cord stimulation (SCS) in painful diabetic peripheral neuropathy (PDPN) is
      not available. We report prospective data on the effect of SCS on pain ratings,
      treatment success and failure, and complications during a 5-year follow-up in
      patients with PDPN. RESEARCH DESIGN AND METHODS: Patients with PDPN (n = 48) were
      included in this prospective multicenter study. The Michigan Diabetic Neuropathy 
      Score (MDNS) was used to assess the severity of neuropathy. Numerical rating
      scale (NRS) score for pain, Patient's Global Impression of Change (PGIC), and
      treatment success (50% reduction of NRS score or significant PGIC) during 5 years
      of follow-up were evaluated. Complications of SCS were reported, and associations
      between baseline characteristics and SCS trial success or failure during a 5-year
      follow-up were investigated by using survival analyses. RESULTS: Treatment
      success was observed in 55% of patients after 5 years. Median duration of SCS
      treatment was 60 months (minimum 1 month, maximum 60 months), and 80% of patients
      with a permanent implant still used their SCS device after 5 years. Higher MDNS
      was associated with treatment failure during the 5-year follow-up (hazard ratio
      3.9 [95% CI 1.3-11.6]; P = 0.014). CONCLUSIONS: SCS is successful in reducing
      chronic pain symptoms in the lower extremities of patients with PDPN up to 5
      years after initiation of treatment. Furthermore, 80% of patients with PDPN still
      use their SCS device after 5 years. Moreover, the severity of neuropathy is
      associated with a higher chance of long-term treatment failure during a 5-year
      follow-up.
CI  - (c) 2017 by the American Diabetes Association.
FAU - van Beek, Maarten
AU  - van Beek M
AUID- ORCID: 0000-0002-4788-6393
AD  - Department of Anesthesiology and Pain Medicine, Maastricht University Medical
      Centre, Maastricht, the Netherlands m.vanbeek@maastrichtuniversity.nl
      maarten.van.kleef@mumc.nl.
FAU - Geurts, Jose W
AU  - Geurts JW
AD  - Department of Anesthesiology and Pain Medicine, Maastricht University Medical
      Centre, Maastricht, the Netherlands.
AD  - Department of Anesthesiology, Rijnstate Hospital, Arnhem, the Netherlands.
FAU - Slangen, Rachel
AU  - Slangen R
AD  - Department of Anesthesiology and Pain Medicine, Maastricht University Medical
      Centre, Maastricht, the Netherlands.
FAU - Schaper, Nicolaas C
AU  - Schaper NC
AD  - Department of Internal Medicine, Maastricht University Medical Centre,
      Maastricht, the Netherlands.
FAU - Faber, Catharina G
AU  - Faber CG
AD  - Department of Neurology, Maastricht University Medical Centre, Maastricht, the
      Netherlands.
FAU - Joosten, Elbert A
AU  - Joosten EA
AD  - Department of Anesthesiology and Pain Medicine, Maastricht University Medical
      Centre, Maastricht, the Netherlands.
FAU - Dirksen, Carmen D
AU  - Dirksen CD
AD  - Department of Clinical Epidemiology and Medical Technology Assessment, Maastricht
      University Medical Centre+, Maastricht, the Netherlands.
AD  - Care and Public Health Research Institute School for Public Health and Primary
      Care, Maastricht University, Maastricht, the Netherlands.
FAU - van Dongen, Robert T
AU  - van Dongen RT
AD  - Department of Anesthesiology, Pain, and Palliative Care, Radboud University
      Medical Centre, Nijmegen, the Netherlands.
FAU - van Kuijk, Sander M J
AU  - van Kuijk SMJ
AD  - Department of Clinical Epidemiology and Medical Technology Assessment, Maastricht
      University Medical Centre+, Maastricht, the Netherlands.
FAU - van Kleef, Maarten
AU  - van Kleef M
AD  - Department of Anesthesiology and Pain Medicine, Maastricht University Medical
      Centre, Maastricht, the Netherlands m.vanbeek@maastrichtuniversity.nl
      maarten.van.kleef@mumc.nl.
LA  - eng
SI  - ClinicalTrials.gov/NCT01162993
SI  - ClinicalTrials.gov/NCT00802022
PT  - Clinical Trial
PT  - Journal Article
PT  - Multicenter Study
PT  - Research Support, Non-U.S. Gov't
DEP - 20171106
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (Glycated Hemoglobin A)
SB  - IM
MH  - Aged
MH  - Chronic Pain
MH  - Cross-Sectional Studies
MH  - Diabetic Neuropathies/*diagnosis/etiology/*therapy
MH  - Female
MH  - Follow-Up Studies
MH  - Glycated Hemoglobin A/metabolism
MH  - Humans
MH  - Male
MH  - Michigan
MH  - Middle Aged
MH  - Pain Management
MH  - Prospective Studies
MH  - Spinal Cord Stimulation/*adverse effects
MH  - Time Factors
MH  - Treatment Outcome
EDAT- 2017/11/08 06:00
MHDA- 2018/05/16 06:00
CRDT- 2017/11/08 06:00
PHST- 2017/05/16 00:00 [received]
PHST- 2017/09/25 00:00 [accepted]
PHST- 2017/11/08 06:00 [pubmed]
PHST- 2018/05/16 06:00 [medline]
PHST- 2017/11/08 06:00 [entrez]
AID - dc17-0983 [pii]
AID - 10.2337/dc17-0983 [doi]
PST - ppublish
SO  - Diabetes Care. 2018 Jan;41(1):32-38. doi: 10.2337/dc17-0983. Epub 2017 Nov 6.

PMID- 29126250
OWN - NLM
STAT- MEDLINE
DCOM- 20171214
LR  - 20180518
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
VI  - 102
IP  - 12
DP  - 2017 Dec 1
TI  - Diabetic Microvascular Disease: An Endocrine Society Scientific Statement.
PG  - 4343-4410
LID - 10.1210/jc.2017-01922 [doi]
AB  - Both type 1 and type 2 diabetes adversely affect the microvasculature in multiple
      organs. Our understanding of the genesis of this injury and of potential
      interventions to prevent, limit, or reverse injury/dysfunction is continuously
      evolving. This statement reviews biochemical/cellular pathways involved in
      facilitating and abrogating microvascular injury. The statement summarizes the
      types of injury/dysfunction that occur in the three classical diabetes
      microvascular target tissues, the eye, the kidney, and the peripheral nervous
      system; the statement also reviews information on the effects of diabetes and
      insulin resistance on the microvasculature of skin, brain, adipose tissue, and
      cardiac and skeletal muscle. Despite extensive and intensive research, it is
      disappointing that microvascular complications of diabetes continue to compromise
      the quantity and quality of life for patients with diabetes. Hopefully, by
      understanding and building on current research findings, we will discover new
      approaches for prevention and treatment that will be effective for future
      generations.
CI  - Copyright (c) 2017 Endocrine Society.
FAU - Barrett, Eugene J
AU  - Barrett EJ
AD  - Division of Endocrinology, Department of Medicine, University of Virginia.
FAU - Liu, Zhenqi
AU  - Liu Z
AD  - Division of Endocrinology, Department of Medicine, University of Virginia.
FAU - Khamaisi, Mogher
AU  - Khamaisi M
AD  - Section of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School.
FAU - King, George L
AU  - King GL
AD  - Section of Vascular Cell Biology, Joslin Diabetes Center, Harvard Medical School.
FAU - Klein, Ronald
AU  - Klein R
AD  - Department of Ophthalmology and Visual Sciences, University of Wisconsin School
      of Medicine and Public Health.
FAU - Klein, Barbara E K
AU  - Klein BEK
AD  - Department of Ophthalmology and Visual Sciences, University of Wisconsin School
      of Medicine and Public Health.
FAU - Hughes, Timothy M
AU  - Hughes TM
AD  - Sticht Center for Healthy Aging and Alzheimer's Prevention, Wake Forest School of
      Medicine.
FAU - Craft, Suzanne
AU  - Craft S
AD  - Sticht Center for Healthy Aging and Alzheimer's Prevention, Wake Forest School of
      Medicine.
FAU - Freedman, Barry I
AU  - Freedman BI
AD  - Divisions of Nephrology and Endocrinology, Department of Internal Medicine,
      Centers for Diabetes Research, and Center for Human Genomics and Personalized
      Medicine Research, Wake Forest School of Medicine.
FAU - Bowden, Donald W
AU  - Bowden DW
AD  - Divisions of Nephrology and Endocrinology, Department of Internal Medicine,
      Centers for Diabetes Research, and Center for Human Genomics and Personalized
      Medicine Research, Wake Forest School of Medicine.
FAU - Vinik, Aaron I
AU  - Vinik AI
AD  - EVMS Strelitz Diabetes Center, Eastern Virginia Medical Center.
FAU - Casellini, Carolina M
AU  - Casellini CM
AD  - EVMS Strelitz Diabetes Center, Eastern Virginia Medical Center.
LA  - eng
GR  - P30 AG049638/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Review
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
SB  - AIM
SB  - IM
MH  - Cerebrovascular Disorders/epidemiology/metabolism/pathology
MH  - Diabetes Mellitus, Type 1/complications
MH  - Diabetes Mellitus, Type 2/complications
MH  - Diabetic Angiopathies/epidemiology/metabolism/*pathology
MH  - Diabetic Nephropathies/epidemiology/metabolism/pathology
MH  - Diabetic Retinopathy/epidemiology/metabolism/pathology
MH  - Humans
MH  - Quality of Life
PMC - PMC5718697
EDAT- 2017/11/11 06:00
MHDA- 2017/12/15 06:00
CRDT- 2017/11/11 06:00
PMCR- 2018/12/01 00:00
PHST- 2017/08/29 00:00 [received]
PHST- 2017/08/29 00:00 [accepted]
PHST- 2018/12/01 00:00 [pmc-release]
PHST- 2017/11/11 06:00 [pubmed]
PHST- 2017/12/15 06:00 [medline]
PHST- 2017/11/11 06:00 [entrez]
AID - 4604942 [pii]
AID - 10.1210/jc.2017-01922 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 2017 Dec 1;102(12):4343-4410. doi:
      10.1210/jc.2017-01922.

PMID- 29126227
OWN - NLM
STAT- MEDLINE
DCOM- 20180521
LR  - 20180521
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
VI  - 103
IP  - 1
DP  - 2018 Jan 1
TI  - Letter to the Editor: "Development and Risk Factors of Type 2 Diabetes in a
      Nationwide Population of Women With Polycystic Ovary Syndrome".
PG  - 360-361
LID - 10.1210/jc.2017-02051 [doi]
FAU - Livadas, Sarantis
AU  - Livadas S
AD  - Endocrine Unit, Metropolitan Hospital, Athens, Greece.
LA  - eng
PT  - Letter
PT  - Comment
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
SB  - AIM
SB  - IM
CON - J Clin Endocrinol Metab. 2017 Oct 1;102(10 ):3848-3857. PMID: 28938447
CIN - J Clin Endocrinol Metab. 2018 Jan 1;103(1):362-363. PMID: 29126200
MH  - *Diabetes Mellitus, Type 2
MH  - Female
MH  - Humans
MH  - Insulin Resistance
MH  - *Polycystic Ovary Syndrome
MH  - Risk Factors
EDAT- 2017/11/11 06:00
MHDA- 2018/05/22 06:00
CRDT- 2017/11/11 06:00
PHST- 2017/09/16 00:00 [received]
PHST- 2017/10/31 00:00 [accepted]
PHST- 2017/11/11 06:00 [pubmed]
PHST- 2018/05/22 06:00 [medline]
PHST- 2017/11/11 06:00 [entrez]
AID - 4590231 [pii]
AID - 10.1210/jc.2017-02051 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 2018 Jan 1;103(1):360-361. doi: 10.1210/jc.2017-02051.

PMID- 29126200
OWN - NLM
STAT- MEDLINE
DCOM- 20180521
LR  - 20180521
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
VI  - 103
IP  - 1
DP  - 2018 Jan 1
TI  - Response to Letter to the Editor: "Development and Risk Factors of Type 2
      Diabetes in a Nationwide Population of Women With Polycystic Ovary Syndrome".
PG  - 362-363
LID - 10.1210/jc.2017-02123 [doi]
FAU - Glintborg, Dorte
AU  - Glintborg D
AD  - Department of Endocrinology, Odense University Hospital, Odense C, Denmark.
FAU - Rubin, Katrine Hass
AU  - Rubin KH
AD  - OPEN-Odense Patient Data Explorative Network, Institute of Clinical Research,
      University of Southern Denmark, Odense C, Denmark.
FAU - Abrahamsen, Bo
AU  - Abrahamsen B
AD  - OPEN-Odense Patient Data Explorative Network, Institute of Clinical Research,
      University of Southern Denmark, Odense C, Denmark.
AD  - Department of Internal Medicine, Holbaek Hospital, Holbaek, Denmark.
FAU - Andersen, Marianne
AU  - Andersen M
AD  - Department of Endocrinology, Odense University Hospital, Odense C, Denmark.
LA  - eng
PT  - Letter
PT  - Comment
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
SB  - AIM
SB  - IM
CON - J Clin Endocrinol Metab. 2017 Oct 1;102(10 ):3848-3857. PMID: 28938447
CON - J Clin Endocrinol Metab. 2018 Jan 1;103(1):360-361. PMID: 29126227
MH  - *Diabetes Mellitus, Type 2
MH  - Female
MH  - Humans
MH  - Insulin Resistance
MH  - *Polycystic Ovary Syndrome
MH  - Risk Factors
EDAT- 2017/11/11 06:00
MHDA- 2018/05/22 06:00
CRDT- 2017/11/11 06:00
PHST- 2017/09/27 00:00 [received]
PHST- 2017/10/31 00:00 [accepted]
PHST- 2017/11/11 06:00 [pubmed]
PHST- 2018/05/22 06:00 [medline]
PHST- 2017/11/11 06:00 [entrez]
AID - 4590232 [pii]
AID - 10.1210/jc.2017-02123 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 2018 Jan 1;103(1):362-363. doi: 10.1210/jc.2017-02123.

PMID- 29126197
OWN - NLM
STAT- MEDLINE
DCOM- 20180626
LR  - 20180626
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
VI  - 103
IP  - 1
DP  - 2018 Jan 1
TI  - Impaired Insulin Action Is Associated With Increased Glucagon Concentrations in
      Nondiabetic Humans.
PG  - 314-319
LID - 10.1210/jc.2017-01197 [doi]
AB  - Context: Abnormal glucagon concentrations contribute to hyperglycemia, but the
      mechanisms of alpha-cell dysfunction in prediabetes are unclear. Objective: We
      sought to determine the relative contributions of insulin secretion and action to
      alpha-cell dysfunction in nondiabetic participants across the spectrum of glucose
      tolerance. Design: This was a cross-sectional study. A subset of participants (n 
      = 120) was studied in the presence and absence of free fatty acid (FFA)
      elevation, achieved by infusion of Intralipid (Baxter Healthcare, Deerfield, IL) 
      plus heparin, to cause insulin resistance. Setting: An inpatient clinical
      research unit at an academic medical center. Participants: A total of 310
      nondiabetic persons participated in this study. Interventions: Participants
      underwent a seven-sample oral glucose tolerance test. Subsequently, 120
      participants were studied on two occasions. On one day, infusion of Intralipid
      plus heparin raised FFA. On the other day, participants received glycerol as a
      control. Main Outcome Measure(s): We examined the relationship of glucagon
      concentration with indices of insulin action after adjusting for the effects of
      age, sex, and weight. Subsequently, we sought to determine whether an acute
      decrease in insulin action, produced by FFA elevation, altered glucagon
      concentrations in nondiabetic participants. Results: Fasting glucagon
      concentrations correlated positively with fasting insulin and C-peptide
      concentrations and inversely with insulin action. Fasting glucagon was not
      associated with any index of beta-cell function in response to an oral challenge.
      As expected, FFA elevation decreased insulin action and also raised glucagon
      concentrations. Conclusions: In nondiabetic participants, glucagon secretion was 
      altered by changes in insulin action.
CI  - Copyright (c) 2017 Endocrine Society
FAU - Sharma, Anu
AU  - Sharma A
AD  - Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of
      Medicine, Rochester, Minnesota.
FAU - Varghese, Ron T
AU  - Varghese RT
AD  - Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of
      Medicine, Rochester, Minnesota.
FAU - Shah, Meera
AU  - Shah M
AD  - Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of
      Medicine, Rochester, Minnesota.
FAU - Man, Chiara Dalla
AU  - Man CD
AD  - Department of Information Engineering, Universita di Padova, Padova, Italy.
FAU - Cobelli, Claudio
AU  - Cobelli C
AD  - Department of Information Engineering, Universita di Padova, Padova, Italy.
FAU - Rizza, Robert A
AU  - Rizza RA
AD  - Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of
      Medicine, Rochester, Minnesota.
FAU - Bailey, Kent R
AU  - Bailey KR
AD  - Biomedical Statistics and Informatics, Mayo Clinic College of Medicine,
      Rochester, Minnesota.
FAU - Vella, Adrian
AU  - Vella A
AD  - Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of
      Medicine, Rochester, Minnesota.
LA  - eng
GR  - R01 DK078646/DK/NIDDK NIH HHS/United States
GR  - R01 DK116231/DK/NIDDK NIH HHS/United States
GR  - T32 DK007352/DK/NIDDK NIH HHS/United States
GR  - UL1 TR000135/TR/NCATS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Biomarkers)
RN  - 0 (Blood Glucose)
RN  - 0 (C-Peptide)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Insulin)
RN  - 9007-92-5 (Glucagon)
SB  - AIM
SB  - IM
MH  - Biomarkers/blood
MH  - Blood Glucose/metabolism
MH  - C-Peptide/blood
MH  - Cross-Sectional Studies
MH  - Female
MH  - Follow-Up Studies
MH  - Glucagon/*blood
MH  - Glucagon-Secreting Cells/drug effects/metabolism/*pathology
MH  - Glucose Tolerance Test
MH  - Humans
MH  - Hyperglycemia/*physiopathology
MH  - Hypoglycemic Agents/pharmacology
MH  - Insulin/*pharmacology
MH  - *Insulin Resistance
MH  - Male
MH  - Middle Aged
MH  - Prediabetic State/*physiopathology
MH  - Prognosis
PMC - PMC5761487
EDAT- 2017/11/11 06:00
MHDA- 2018/06/27 06:00
CRDT- 2017/11/11 06:00
PMCR- 2019/01/01 00:00
PHST- 2017/05/25 00:00 [received]
PHST- 2017/11/01 00:00 [accepted]
PHST- 2019/01/01 00:00 [pmc-release]
PHST- 2017/11/11 06:00 [pubmed]
PHST- 2018/06/27 06:00 [medline]
PHST- 2017/11/11 06:00 [entrez]
AID - 4590235 [pii]
AID - 10.1210/jc.2017-01197 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 2018 Jan 1;103(1):314-319. doi: 10.1210/jc.2017-01197.