PMID- 30837211
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20190409
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Linking)
VI  - 364
DP  - 2019 Mar 5
TI  - Questions over future of global diabetes group as founding members resign.
PG  - l995
LID - 10.1136/bmj.l995 [doi]
FAU - Newman, Melanie
AU  - Newman M
LA  - eng
PT  - Journal Article
DEP - 20190305
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
COIS- Competing interests: I have read and understood BMJ policy on declaration of
      interests and have no relevant interests to declare.
EDAT- 2019/03/07 06:00
MHDA- 2019/03/07 06:01
CRDT- 2019/03/07 06:00
PHST- 2019/03/07 06:00 [entrez]
PHST- 2019/03/07 06:00 [pubmed]
PHST- 2019/03/07 06:01 [medline]
AID - 10.1136/bmj.l995 [doi]
PST - epublish
SO  - BMJ. 2019 Mar 5;364:l995. doi: 10.1136/bmj.l995.

PMID- 30848534
OWN - NLM
STAT- In-Data-Review
LR  - 20190308
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 36
IP  - 4
DP  - 2019 Apr
TI  - Predicting the future: Diabetes and Brexit.
PG  - 397-398
LID - 10.1111/dme.13938 [doi]
FAU - Holt, Richard I G
AU  - Holt RIG
AD  - University of Southampton.
LA  - eng
PT  - Editorial
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
EDAT- 2019/03/09 06:00
MHDA- 2019/03/09 06:00
CRDT- 2019/03/09 06:00
PHST- 2019/03/09 06:00 [entrez]
PHST- 2019/03/09 06:00 [pubmed]
PHST- 2019/03/09 06:00 [medline]
AID - 10.1111/dme.13938 [doi]
PST - ppublish
SO  - Diabet Med. 2019 Apr;36(4):397-398. doi: 10.1111/dme.13938.

PMID- 30848519
OWN - NLM
STAT- Publisher
LR  - 20190405
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
DP  - 2019 Mar 8
TI  - Impact of glycaemic control on fracture risk in 5368 people with newly diagnosed 
      Type 1 diabetes: a time-dependent analysis.
LID - 10.1111/dme.13945 [doi]
AB  - AIMS: To assess whether glycaemic control is associated with a lifelong increased
      risk of fracture in people with newly diagnosed Type 1 diabetes. METHODS: People 
      with newly diagnosed Type 1 diabetes between 1 January 1995 and 10 May 2016 were 
      identified in The Health Improvement Network database. Longitudinal HbA1c
      measurements from diagnosis to fracture or study end or loss to follow-up were
      collected. A Cox proportional hazards model with HbA1c included as a
      time-dependent variable was fitted to these data. RESULTS: Some 5368 people with 
      newly diagnosed Type 1 diabetes were included. The estimated adjusted hazard
      ratio (aHR) for HbA1c was statistically significant [aHR 1.007; 95% confidence
      interval (CI) 1.002-1.011 (mmol/mol) and aHR 1.07; 95% CI 1.03-1.12 (%)]. An
      incremental higher risk of fracture was observed with increasing levels of HbA1c 
      . CONCLUSIONS: In people with newly diagnosed Type 1 diabetes, higher HbA1c is
      associated with an increased risk for fractures.
CI  - (c) 2019 Diabetes UK.
FAU - Thayakaran, R
AU  - Thayakaran R
AD  - Institute of Applied Health Research, University of Birmingham, Birmingham, UK.
FAU - Perrins, M
AU  - Perrins M
AD  - Institute of Applied Health Research, University of Birmingham, Birmingham, UK.
FAU - Gokhale, K M
AU  - Gokhale KM
AD  - Institute of Applied Health Research, University of Birmingham, Birmingham, UK.
FAU - Kumaran, S
AU  - Kumaran S
AD  - Institute of Applied Health Research, University of Birmingham, Birmingham, UK.
FAU - Narendran, P
AU  - Narendran P
AUID- ORCID: https://orcid.org/0000-0002-4583-8793
AD  - Department of Diabetes, University Hospitals Birmingham NHS Foundation Trust,
      Birmingham, UK.
AD  - Institute of Immunology and Immunotherapy, Birmingham, UK.
FAU - Price, M J
AU  - Price MJ
AD  - Institute of Applied Health Research, University of Birmingham, Birmingham, UK.
AD  - NIHR Birmingham Biomedical Research Centre, University Hospitals Birmingham NHS
      Foundation Trust and University of Birmingham, Birmingham, UK.
FAU - Nirantharakumar, K
AU  - Nirantharakumar K
AD  - Institute of Applied Health Research, University of Birmingham, Birmingham, UK.
AD  - Department of Diabetes, University Hospitals Birmingham NHS Foundation Trust,
      Birmingham, UK.
AD  - Centre for Endocrinology, Diabetes and Metabolism, University of Birmingham,
      Birmingham, UK.
AD  - Health Data Research UK Midlands, Birmingham, UK.
FAU - Toulis, K A
AU  - Toulis KA
AUID- ORCID: https://orcid.org/0000-0002-2044-4253
AD  - Institute of Applied Health Research, University of Birmingham, Birmingham, UK.
LA  - eng
PT  - Journal Article
DEP - 20190308
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
EDAT- 2019/03/09 06:00
MHDA- 2019/03/09 06:00
CRDT- 2019/03/09 06:00
PHST- 2019/03/05 00:00 [accepted]
PHST- 2019/03/09 06:00 [pubmed]
PHST- 2019/03/09 06:00 [medline]
PHST- 2019/03/09 06:00 [entrez]
AID - 10.1111/dme.13945 [doi]
PST - aheadofprint
SO  - Diabet Med. 2019 Mar 8. doi: 10.1111/dme.13945.

PMID- 30838691
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20190319
IS  - 1464-5491 (Electronic)
IS  - 0742-3071 (Linking)
VI  - 36 Suppl 1
DP  - 2019 Mar
TI  - Abstracts of the Diabetes UK Professional Conference 2019, ACC Liverpool,
      Liverpool, 6-8 March 2019.
PG  - 5-174
LID - 10.1111/dme.13882 [doi]
LA  - eng
PT  - Journal Article
PL  - England
TA  - Diabet Med
JT  - Diabetic medicine : a journal of the British Diabetic Association
JID - 8500858
EDAT- 2019/03/07 06:00
MHDA- 2019/03/07 06:01
CRDT- 2019/03/07 06:00
PHST- 2019/03/07 06:00 [entrez]
PHST- 2019/03/07 06:00 [pubmed]
PHST- 2019/03/07 06:01 [medline]
AID - 10.1111/dme.13882 [doi]
PST - ppublish
SO  - Diabet Med. 2019 Mar;36 Suppl 1:5-174. doi: 10.1111/dme.13882.

PMID- 30833470
OWN - NLM
STAT- Publisher
LR  - 20190305
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2019 Mar 4
TI  - HLA Class II Antigen Processing and Presentation Pathway Components Demonstrated 
      by Transcriptome and Protein Analyses of islet beta-Cells from Donors with Type 1
      Diabetes.
LID - db180686 [pii]
LID - 10.2337/db18-0686 [doi]
AB  - Type 1 diabetes studies consistently generate data showing islet beta-cell
      dysfunction and T-cell mediated anti-beta-cell specific autoimmunity. To explore 
      the pathogenesis, we interrogated the beta-cell transcriptomes from donors with
      and without type 1 diabetes using both bulk-sorted and single beta-cells.
      Consistent with immunohistological studies, beta-cells from donors with type 1
      diabetes displayed increased Class I transcripts and associated mRNA species.
      These beta-cells also expressed mRNA for Class II and Class II antigen
      presentation pathway components, but lacked macrophage marker, CD68.
      Immunohistological study of three independent recent-onset type 1 diabetic donor 
      cohorts showed Class II protein and its transcriptional regulator Class II major 
      histocompatibility complex trans-activator (CIITA) protein expressed by a subset 
      of insulin(+) CD68(-) beta-cells, specifically found in islets with lymphocytic
      infiltrates. beta-cell surface expression of HLA Class II was detected on a
      portion of CD45(-)insulin(+) beta-cells from donors with type 1 diabetes by
      immunofluorescence and flow cytometry. Our data demonstrate that pancreatic
      beta-cells from donors with type 1 diabetes express Class II molecules on
      selected cells with other key genes in those pathways and inflammation-associated
      genes. beta-cell expression of Class II molecules suggests that beta-cells may
      interact directly with islet-infiltrating CD4(+) T-cells, and may play an
      immunopathogenic role.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Russell, Mark A
AU  - Russell MA
AD  - Institute of Biomedical & Clinical Science, University of Exeter Medical School, 
      Exeter, Devon, UK.
FAU - Redick, Sambra D
AU  - Redick SD
AD  - Program in Molecular Medicine, Diabetes Center of Excellence, University of
      Massachusetts Medical School, Worcester, MA, USA.
FAU - Blodgett, David M
AU  - Blodgett DM
AD  - Department of Medicine, Division of Diabetes, Diabetes Center of Excellence,
      University of Massachusetts Medical School, Worcester, MA, USA.
AD  - Math and Science Division, Babson College, Wellesley, MA, USA.
FAU - Richardson, Sarah J
AU  - Richardson SJ
AD  - Institute of Biomedical & Clinical Science, University of Exeter Medical School, 
      Exeter, Devon, UK.
FAU - Leete, Pia
AU  - Leete P
AD  - Institute of Biomedical & Clinical Science, University of Exeter Medical School, 
      Exeter, Devon, UK.
FAU - Krogvold, Lars
AU  - Krogvold L
AD  - Pediatric Department, Oslo University Hospital, Oslo, Norway and Faculty of
      Medicine, University of Oslo, Oslo, Norway.
FAU - Dahl-Jorgensen, Knut
AU  - Dahl-Jorgensen K
AD  - Pediatric Department, Oslo University Hospital, Oslo, Norway and Faculty of
      Medicine, University of Oslo, Oslo, Norway.
FAU - Bottino, Rita
AU  - Bottino R
AD  - Institute of Cellular Therapeutics, Allegheny-Singer Research Institute
      Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA,
      USA.
FAU - Brissova, Marcela
AU  - Brissova M
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Medicine,
      Vanderbilt University Medical Center, Nashville, TN, USA.
FAU - Spaeth, Jason M
AU  - Spaeth JM
AD  - Department of Molecular Physiology and Biophysics, Vanderbilt University,
      Nashville, TN, USA.
FAU - Babon, Jenny Aurielle B
AU  - Babon JAB
AD  - Department of Medicine, Division of Diabetes, Diabetes Center of Excellence,
      University of Massachusetts Medical School, Worcester, MA, USA.
FAU - Haliyur, Rachana
AU  - Haliyur R
AD  - Department of Molecular Physiology and Biophysics, Vanderbilt University,
      Nashville, TN, USA.
FAU - Powers, Alvin C
AU  - Powers AC
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Medicine,
      Vanderbilt University Medical Center, Nashville, TN, USA.
AD  - Department of Molecular Physiology and Biophysics, Vanderbilt University,
      Nashville, TN, USA.
AD  - Veterans Affairs Tennessee Valley Healthcare System, Nashville, TN, USA.
FAU - Yang, Chaoxing
AU  - Yang C
AD  - Program in Molecular Medicine, Diabetes Center of Excellence, University of
      Massachusetts Medical School, Worcester, MA, USA.
FAU - Kent, Sally C
AU  - Kent SC
AD  - Department of Medicine, Division of Diabetes, Diabetes Center of Excellence,
      University of Massachusetts Medical School, Worcester, MA, USA.
FAU - Derr, Alan G
AU  - Derr AG
AD  - Program in Bioinformatics, University of Massachusetts Medical School Worcester, 
      MA, USA.
FAU - Kucukural, Alper
AU  - Kucukural A
AD  - Program in Bioinformatics, University of Massachusetts Medical School Worcester, 
      MA, USA.
FAU - Garber, Manuel G
AU  - Garber MG
AD  - Program in Bioinformatics, University of Massachusetts Medical School Worcester, 
      MA, USA.
FAU - Morgan, Noel G
AU  - Morgan NG
AD  - Institute of Biomedical & Clinical Science, University of Exeter Medical School, 
      Exeter, Devon, UK.
FAU - Harlan, David M
AU  - Harlan DM
AD  - Department of Medicine, Division of Diabetes, Diabetes Center of Excellence,
      University of Massachusetts Medical School, Worcester, MA, USA
      David.Harlan@umassmemorial.org.
LA  - eng
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/06/20 00:00 [received]
PHST- 2019/02/25 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - db18-0686 [pii]
AID - 10.2337/db18-0686 [doi]
PST - aheadofprint
SO  - Diabetes. 2019 Mar 4. pii: db18-0686. doi: 10.2337/db18-0686.

PMID- 30833469
OWN - NLM
STAT- Publisher
LR  - 20190305
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2019 Mar 4
TI  - Fasting-Induced Transcription Factors Repress Vitamin D Bioactivation, a
      Mechanism for Vitamin D Deficiency in Diabetes.
LID - db181050 [pii]
LID - 10.2337/db18-1050 [doi]
AB  - Low 25-hydroxyvitamin D levels correlate with the prevalence of diabetes,
      however, the mechanisms remain uncertain. Here, we show that nutritional
      deprivation responsive mechanisms regulate vitamin D metabolism. Both fasting and
      diabetes suppressed hepatic cytochrome P450 (CYP) 2R1, the main vitamin D
      25-hydroxylase, responsible for the first bioactivation step. Overexpression of
      coactivator peroxisome proliferator-activated receptor gamma coactivator 1-alpha 
      (PGC-1alpha), induced physiologically by fasting and pathologically in diabetes, 
      resulted in dramatic downregulation of CYP2R1 in mouse hepatocytes in an
      estrogen-related receptor alpha (ERRalpha)-dependent manner. However, PGC-1alpha 
      knockout did not prevent fasting-induced suppression of CYP2R1 in the liver
      indicating that additional factors contribute to the CYP2R1 repression.
      Furthermore, glucocorticoid receptor (GR) activation repressed the liver CYP2R1, 
      suggesting GR involvement in the regulation of CYP2R1. GR antagonist mifepristone
      partially prevented CYP2R1 repression during fasting suggesting that
      glucocorticoids and GR contribute to the CYP2R1 repression during fasting.
      Moreover, fasting upregulated the vitamin D catabolizing CYP24A1 in the kidney
      through the PGC-1alpha-ERRalpha pathway. Our study uncovers a molecular mechanism
      for vitamin D deficiency in diabetics and reveals a novel negative feedback
      mechanism controlling cross-talk between energy homeostasis and the vitamin D
      pathway.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Aatsinki, Sanna-Mari
AU  - Aatsinki SM
AD  - Research Unit of Biomedicine, Pharmacology and Toxicology, University of Oulu,
      Oulu, Finland.
AD  - Medical Research Center Oulu, Oulu University Hospital and University of Oulu,
      Oulu, Finland.
AD  - Admescope Ltd., Typpitie 1, 90620 Oulu, Finland.
FAU - Elkhwanky, Mahmoud-Sobhy
AU  - Elkhwanky MS
AD  - Research Unit of Biomedicine, Pharmacology and Toxicology, University of Oulu,
      Oulu, Finland.
AD  - Medical Research Center Oulu, Oulu University Hospital and University of Oulu,
      Oulu, Finland.
FAU - Kummu, Outi
AU  - Kummu O
AD  - Research Unit of Biomedicine, Pharmacology and Toxicology, University of Oulu,
      Oulu, Finland.
AD  - Medical Research Center Oulu, Oulu University Hospital and University of Oulu,
      Oulu, Finland.
FAU - Karpale, Mikko
AU  - Karpale M
AD  - Research Unit of Biomedicine, Pharmacology and Toxicology, University of Oulu,
      Oulu, Finland.
AD  - Medical Research Center Oulu, Oulu University Hospital and University of Oulu,
      Oulu, Finland.
FAU - Buler, Marcin
AU  - Buler M
AD  - Research Unit of Biomedicine, Pharmacology and Toxicology, University of Oulu,
      Oulu, Finland.
AD  - Medical Research Center Oulu, Oulu University Hospital and University of Oulu,
      Oulu, Finland.
FAU - Viitala, Pirkko
AU  - Viitala P
AD  - Research Unit of Biomedicine, Pharmacology and Toxicology, University of Oulu,
      Oulu, Finland.
FAU - Rinne, Valtteri
AU  - Rinne V
AD  - Admescope Ltd., Typpitie 1, 90620 Oulu, Finland.
FAU - Mutikainen, Maija
AU  - Mutikainen M
AD  - A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland,
      Kuopio, Finland.
FAU - Tavi, Pasi
AU  - Tavi P
AD  - A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland,
      Kuopio, Finland.
FAU - Franko, Andras
AU  - Franko A
AD  - Vegetative Physiology, Medical Faculty, University of Koln, Koln, Germany.
AD  - Institute for Clinical Chemistry and Pathobiochemistry, Department for Diagnostic
      Laboratory Medicine, University Hospital Tuebingen, 72076 Tuebingen, Germany.
AD  - German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany.
FAU - Wiesner, Rudolf J
AU  - Wiesner RJ
AD  - Vegetative Physiology, Medical Faculty, University of Koln, Koln, Germany.
FAU - Chambers, Kari T
AU  - Chambers KT
AD  - Department of Medicine, Washington University School of Medicine, St. Louis,
      Missouri, United States of America.
FAU - Finck, Brian N
AU  - Finck BN
AD  - Department of Medicine, Washington University School of Medicine, St. Louis,
      Missouri, United States of America.
FAU - Hakkola, Jukka
AU  - Hakkola J
AD  - Research Unit of Biomedicine, Pharmacology and Toxicology, University of Oulu,
      Oulu, Finland jukka.hakkola@oulu.fi.
AD  - Medical Research Center Oulu, Oulu University Hospital and University of Oulu,
      Oulu, Finland.
LA  - eng
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/09/28 00:00 [received]
PHST- 2019/02/26 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - db18-1050 [pii]
AID - 10.2337/db18-1050 [doi]
PST - aheadofprint
SO  - Diabetes. 2019 Mar 4. pii: db18-1050. doi: 10.2337/db18-1050.

PMID- 30833467
OWN - NLM
STAT- Publisher
LR  - 20190329
IS  - 1939-327X (Electronic)
IS  - 0012-1797 (Linking)
DP  - 2019 Mar 4
TI  - Loss-of-Function Mutation in Thiamine Transporter 1 in a Family with Autosomal
      Dominant Diabetes.
LID - db170821 [pii]
LID - 10.2337/db17-0821 [doi]
AB  - Solute Carrier Family 19 Member 2 (SLC19A2) encodes thiamine transporter 1
      (THTR1), which facilitates thiamine transport across the cell membrane. SLC19A2
      homozygous mutations have been described as a cause of thiamine-responsive
      megaloblastic anemia (TRMA), an autosomal recessive syndrome characterized by
      megaloblastic anemia, diabetes mellitus, and sensorineural deafness. Here we
      describe a loss-of-function SLC19A2 mutation (c.A1063C: p.Lys355Gln) in a family 
      with early-onset diabetes and mild TRMA traits transmitted in an autosomal
      dominant fashion. We show that SLC19A2 deficient beta-cells are characterized by 
      impaired thiamine uptake, which is not rescued by overexpression of the
      p.Lys355Gln mutant protein. We further demonstrate that SLC19A2 deficit causes
      impaired insulin secretion in conjunction with mitochondrial dysfunction, loss of
      protection against oxidative stress, and cell cycle arrest. These findings link
      SLC19A2 mutations to autosomal dominant diabetes and suggest a role of SLC19A2 in
      beta-cell function and survival.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Jungtrakoon, Prapaporn
AU  - Jungtrakoon P
AD  - Department of Medicine, Harvard Medical School, Boston, MA, 02215, USA.
AD  - Section on Genetics and Epidemiology, Joslin Diabetes Center, Boston, MA, 02215, 
      USA.
AD  - Division of Molecular Medicine, Research Department, Faculty of Medicine Siriraj 
      Hospital, Mahidol University, Bangkok, 10700, Thailand.
FAU - Shirakawa, Jun
AU  - Shirakawa J
AD  - Department of Medicine, Harvard Medical School, Boston, MA, 02215, USA.
AD  - Section on Islet Cell and Regenerative Biology, Joslin Diabetes Center, Boston,
      MA, 02215, USA.
FAU - Buranasupkajorn, Patinut
AU  - Buranasupkajorn P
AD  - Department of Medicine, Harvard Medical School, Boston, MA, 02215, USA.
AD  - Section on Genetics and Epidemiology, Joslin Diabetes Center, Boston, MA, 02215, 
      USA.
AD  - Division of Hospital and Ambulatory Medicine, Department of Medicine, Faculty of 
      Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
FAU - Gupta, Manoj K
AU  - Gupta MK
AD  - Department of Medicine, Harvard Medical School, Boston, MA, 02215, USA.
AD  - Section on Islet Cell and Regenerative Biology, Joslin Diabetes Center, Boston,
      MA, 02215, USA.
FAU - De Jesus, Dario F
AU  - De Jesus DF
AD  - Department of Medicine, Harvard Medical School, Boston, MA, 02215, USA.
AD  - Section on Islet Cell and Regenerative Biology, Joslin Diabetes Center, Boston,
      MA, 02215, USA.
FAU - Pezzolesi, Marcus G
AU  - Pezzolesi MG
AD  - Division of Nephrology and Hypertension, University of Utah School of Medicine,
      Salt Lake City, UT, 84105, USA.
FAU - Panya, Aussara
AU  - Panya A
AD  - Department of Medicine, Harvard Medical School, Boston, MA, 02215, USA.
AD  - Section on Genetics and Epidemiology, Joslin Diabetes Center, Boston, MA, 02215, 
      USA.
AD  - Division of Molecular Medicine, Research Department, Faculty of Medicine Siriraj 
      Hospital, Mahidol University, Bangkok, 10700, Thailand.
FAU - Hastings, Timothy
AU  - Hastings T
AD  - Section on Genetics and Epidemiology, Joslin Diabetes Center, Boston, MA, 02215, 
      USA.
FAU - Chanprasert, Chutima
AU  - Chanprasert C
AD  - Division of Molecular Medicine, Research Department, Faculty of Medicine Siriraj 
      Hospital, Mahidol University, Bangkok, 10700, Thailand.
FAU - Mendonca, Christine
AU  - Mendonca C
AD  - Section on Genetics and Epidemiology, Joslin Diabetes Center, Boston, MA, 02215, 
      USA.
FAU - Kulkarni, Rohit N
AU  - Kulkarni RN
AD  - Department of Medicine, Harvard Medical School, Boston, MA, 02215, USA.
AD  - Section on Islet Cell and Regenerative Biology, Joslin Diabetes Center, Boston,
      MA, 02215, USA.
FAU - Doria, Alessandro
AU  - Doria A
AD  - Department of Medicine, Harvard Medical School, Boston, MA, 02215, USA.
      alessandro.doria@joslin.harvard.edu.
AD  - Section on Genetics and Epidemiology, Joslin Diabetes Center, Boston, MA, 02215, 
      USA.
LA  - eng
GR  - P30 DK036836/DK/NIDDK NIH HHS/United States
GR  - R01 DK055523/DK/NIDDK NIH HHS/United States
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2017/07/12 00:00 [received]
PHST- 2019/02/23 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - db17-0821 [pii]
AID - 10.2337/db17-0821 [doi]
PST - aheadofprint
SO  - Diabetes. 2019 Mar 4. pii: db17-0821. doi: 10.2337/db17-0821.

PMID- 30833375
OWN - NLM
STAT- Publisher
LR  - 20190305
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Mar 4
TI  - Self-Monitoring of Blood Glucose in Youth-Onset Type 2 Diabetes: Results From the
      TODAY Study.
LID - dc181854 [pii]
LID - 10.2337/dc18-1854 [doi]
AB  - OBJECTIVE: To determine whether self-monitoring of blood glucose (SMBG) is
      associated with lower HbA1c in youth with type 2 diabetes taking oral medications
      only or after starting insulin for persistently elevated HbA1c. RESEARCH DESIGN
      AND METHODS: TODAY participants (n = 699) taking oral medications were asked to
      perform SMBG twice daily. After reaching primary outcome (PO) (HbA1c >/=8% [64
      mmol/mol]) over 6 months or an inability to wean from temporary insulin because
      of metabolic decompensation), insulin glargine was started. HbA1c and percent of 
      SMBG (SMBG%) (percent days when the meter was used one or more times) before and 
      after PO were analyzed. RESULTS: SMBG declined over time and was inversely
      related to HbA1c (P < 0.0001). Of 298 youth who reached PO and started insulin,
      282 had SMBG data. At PO, mean +/- SD age was 15.8 +/- 2.3 years, BMI 35.5 +/-
      7.9 kg/m(2), and HbA1c 9.6 +/- 2.0% (81 +/- 21.9 mmol/mol); 65.3% were female.
      Median SMBG% was 40% at PO, which increased to 49% after 6 months and fell to 41%
      after 1 year on insulin. At PO, 22% of youth checked >/=80% of days, which
      increased to 25% and fell to 19% after 6 and 12 months using insulin,
      respectively. At PO, compared with those who checked <80%, youth who checked
      >/=80% were younger and with a lower BMI, HbA1c, and blood pressure. SMBG >/=80% 
      was associated with >/=1% reduction in HbA1c at 6 and 12 months after insulin
      initiation. CONCLUSIONS: Low SMBG adherence was common and associated with higher
      HbA1c. Optimal SMBG frequency in youth using or not using insulin, and whether
      less frequent SMBG is a marker for overall worse self-care, require further
      study.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Weinstock, Ruth S
AU  - Weinstock RS
AD  - State University of New York Upstate Medical University, Syracuse, NY.
FAU - Braffett, Barbara H
AU  - Braffett BH
AUID- ORCID: http://orcid.org/0000-0002-2184-9754
AD  - The Biostatistics Center, George Washington University, Rockville, MD
      braffett@bsc.gwu.edu.
FAU - McGuigan, Paul
AU  - McGuigan P
AD  - Case Western Reserve University, Rainbow Babies and Children's Hospital,
      Cleveland, OH.
FAU - Larkin, Mary E
AU  - Larkin ME
AD  - Massachusetts General Hospital Diabetes Center, Harvard Medical School, Boston,
      MA.
FAU - Grover, Nisha B
AU  - Grover NB
AD  - The Biostatistics Center, George Washington University, Rockville, MD.
FAU - Walders-Abramson, Natalie
AU  - Walders-Abramson N
AD  - University of Colorado School of Medicine, Aurora, CO.
FAU - Laffel, Lori M
AU  - Laffel LM
AUID- ORCID: http://orcid.org/0000-0002-9675-3001
AD  - Joslin Diabetes Center, Harvard Medical School, Boston, MA.
FAU - Chan, Christine L
AU  - Chan CL
AUID- ORCID: http://orcid.org/0000-0003-3067-7672
AD  - University of Colorado School of Medicine, Aurora, CO.
FAU - Chang, Nancy
AU  - Chang N
AD  - Children's Hospital of Los Angeles, Los Angeles, CA.
FAU - Schwartzman, Beth E
AU  - Schwartzman BE
AD  - Children's Hospital of Philadelphia, Philadelphia, PA.
FAU - Barajas, Rose Ann
AU  - Barajas RA
AD  - University of Texas Health Science Center San Antonio, San Antonio, TX.
FAU - Celona-Jacobs, Nicole
AU  - Celona-Jacobs N
AD  - University of Colorado School of Medicine, Aurora, CO.
FAU - Haymond, Morey W
AU  - Haymond MW
AUID- ORCID: http://orcid.org/0000-0003-0631-2913
CN  - TODAY Study Group
LA  - eng
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/09/04 00:00 [received]
PHST- 2019/02/04 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - dc18-1854 [pii]
AID - 10.2337/dc18-1854 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Mar 4. pii: dc18-1854. doi: 10.2337/dc18-1854.

PMID- 30833374
OWN - NLM
STAT- Publisher
LR  - 20190305
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Mar 4
TI  - Importance of Treatment Status in Links Between Type 2 Diabetes and Alzheimer
      Disease.
LID - dc181399 [pii]
LID - 10.2337/dc18-1399 [doi]
AB  - OBJECTIVE: To investigate relationships among type 2 diabetes treatment,
      Alzheimer disease biomarkers, and risk for dementia. RESEARCH DESIGN AND METHODS:
      Participants from the Alzheimer Disease Neuroimaging Initiative (N = 1,289) who
      were dementia-free at baseline and underwent health assessment, cognitive
      testing, and MRI. A subset (n = 900) obtained a lumbar puncture to determine
      cerebrospinal fluid (CSF) phosphorylated tau (p-tau), total tau (t-tau), and
      beta-amyloid 1-42 (Abeta1-42). Participants were grouped by fasting blood glucose
      and medication history: euglycemia (EU), prediabetes (PD), untreated diabetes
      (UD), and treated diabetes (TD). Relationships were investigated between
      treatment status and CSF biomarkers and risk for dementia. RESULTS: The UD group 
      displayed greater p-tau, t-tau, and p-tau/Abeta1-42 levels than the EU, PD, and
      TD groups (P values <0.05) and higher t-tau/Abeta1-42 than the EU and PD groups
      (P values <0.05). The UD group progressed to dementia at higher rates than the EU
      group (hazard ratio 1.602 [95% CI 1.057-2.429]; P = 0.026). CONCLUSIONS:
      Treatment status may alter the relationship between type 2 diabetes and both
      Alzheimer disease biomarker profile and risk for dementia. UD is associated with 
      elevated tau pathology and risk for dementia, whereas TD is not. Although this
      study is observational and therefore causality cannot be inferred, findings
      support the potential importance of treatment status in Alzheimer disease risk
      associated with type 2 diabetes.
CI  - (c) 2019 by the American Diabetes Association.
FAU - McIntosh, Elissa C
AU  - McIntosh EC
AD  - Department of Psychology, University of Southern California, Los Angeles, CA
      danation@usc.edu ecmcinto@usc.edu.
FAU - Nation, Daniel A
AU  - Nation DA
AUID- ORCID: http://orcid.org/0000-0002-9123-0658
CN  - Alzheimer's Disease Neuroimaging Initiative
LA  - eng
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/06/29 00:00 [received]
PHST- 2019/02/07 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - dc18-1399 [pii]
AID - 10.2337/dc18-1399 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Mar 4. pii: dc18-1399. doi: 10.2337/dc18-1399.

PMID- 30833373
OWN - NLM
STAT- Publisher
LR  - 20190305
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Mar 4
TI  - Long-term Association of Depression Symptoms and Antidepressant Medication Use
      With Incident Cardiovascular Events in the Look AHEAD (Action for Health in
      Diabetes) Clinical Trial of Weight Loss in Type 2 Diabetes.
LID - dc180575 [pii]
LID - 10.2337/dc18-0575 [doi]
AB  - OBJECTIVE: To examine whether depression symptoms or antidepressant medication
      (ADM) use predicts the probability of cardiovascular events in overweight/obese
      individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS: Preplanned
      analyses of depression and incident cardiovascular disease (CVD) were performed
      in the Look AHEAD (Action for Health in Diabetes) weight loss trial after a
      median follow-up of 9.6 years. Depression symptoms, assessed with the Beck
      Depression Inventory (BDI), were analyzed both as a continuous and dichotomized
      variable (BDI score <10 or >/=10). ADM use was coded from participants'
      prescription medications. Four composite CVD outcomes were defined in the study
      protocol. Sex-stratified Cox proportional hazards models were adjusted for a
      range of baseline covariates. RESULTS: Depression symptoms were only
      significantly associated with a composite secondary outcome comprising CVD death,
      nonfatal myocardial infarction, nonfatal stroke, hospitalized angina, congestive 
      heart failure, peripheral vascular disease, coronary artery bypass graft, and
      carotid endarterectomy. Significant sex interactions were observed for BDI score 
      and BDI score >/=10. BDI score was significantly associated with higher
      probability of this composite outcome in men, but was not associated with the
      outcome in women. BDI score >/=10 was positively associated with this composite
      outcome in men but was negatively associated in women. Exploratory analysis
      identified a significant BDI >/=10 x ADM use interaction for this composite
      outcome that differed in men versus women. Men with both BDI score >/=10 and ADM 
      use compared with those with neither had 60% higher probability of the outcome,
      whereas women with both compared with those with neither had 50% lower
      probability. CONCLUSIONS: Sex differences in the association of depression
      symptoms and ADM use with incident CVD warrant further investigation.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Hazuda, Helen P
AU  - Hazuda HP
AUID- ORCID: http://orcid.org/0000-0002-7313-4160
AD  - The University of Texas Health Science Center at San Antonio, San Antonio, TX
      hazuda@uthscsa.edu.
FAU - Gaussoin, Sarah A
AU  - Gaussoin SA
AD  - Wake Forest School of Medicine, Winston-Salem, NC.
FAU - Wing, Rena R
AU  - Wing RR
AD  - The Miriam Hospital/Brown Medical School, Providence, RI.
FAU - Yanovski, Susan Z
AU  - Yanovski SZ
AD  - National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD.
FAU - Johnson, Karen C
AU  - Johnson KC
AD  - The University of Tennessee, Memphis, TN.
FAU - Coday, Mace
AU  - Coday M
AD  - The University of Tennessee, Memphis, TN.
FAU - Wadden, Thomas A
AU  - Wadden TA
AD  - University of Pennsylvania, Philadelphia, PA.
FAU - Horton, Edward S
AU  - Horton ES
AUID- ORCID: http://orcid.org/0000-0002-5670-3157
AD  - Joslin Diabetes Center, Boston, MA.
FAU - Van Dorsten, Brent
AU  - Van Dorsten B
AD  - Colorado Center for Behavioral Medicine, Denver, CO.
FAU - Knowler, William C
AU  - Knowler WC
AUID- ORCID: http://orcid.org/0000-0002-7004-5197
AD  - National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD.
CN  - Look AHEAD Research Group
LA  - eng
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/03/15 00:00 [received]
PHST- 2019/02/07 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - dc18-0575 [pii]
AID - 10.2337/dc18-0575 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Mar 4. pii: dc18-0575. doi: 10.2337/dc18-0575.

PMID- 30833372
OWN - NLM
STAT- Publisher
LR  - 20190305
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Mar 4
TI  - Nonproteinuric Versus Proteinuric Phenotypes in Diabetic Kidney Disease: A
      Propensity Score-Matched Analysis of a Nationwide, Biopsy-Based Cohort Study.
LID - dc181320 [pii]
LID - 10.2337/dc18-1320 [doi]
AB  - OBJECTIVE: Clinicopathological characteristics, renal prognosis, and mortality in
      patients with type 2 diabetes and reduced renal function without overt
      proteinuria are scarce. RESEARCH DESIGN AND METHODS: We retrospectively assessed 
      526 patients with type 2 diabetes and reduced renal function (estimated
      glomerular filtration rate [eGFR] <60 mL/min/1.73 m(2)), who underwent clinical
      renal biopsy and had follow-up data, from Japan's nationwide multicenter renal
      biopsy registry. For comparative analyses, we derived one-to-two cohorts of those
      without proteinuria versus those with proteinuria using propensity score-matching
      methods addressing the imbalances of age, sex, diabetes duration, and baseline
      eGFR. The primary end point was progression of chronic kidney disease (CKD)
      defined as new-onset end-stage renal disease, decrease of eGFR by >/=50%, or
      doubling of serum creatinine. The secondary end point was all-cause mortality.
      RESULTS: Eighty-two patients with nonproteinuria (urine albumin-to-creatinine
      ratio [UACR] <300 mg/g) had lower systolic blood pressure and less-severe
      pathological lesions compared with 164 propensity-matched patients with
      proteinuria (UACR >/=300 mg/g). After a median follow-up of 1.9 years
      (interquartile range 0.9-5.0 years) from the date of renal biopsy, the 5-year CKD
      progression-free survival was 86.6% (95% CI 72.5-93.8%) for the nonproteinuric
      group and 30.3% (95% CI 22.4-38.6%) for the proteinuric group (log-rank test P < 
      0.001). The lower renal risk was consistent across all subgroup analyses. The
      all-cause mortality was also lower in the nonproteinuric group (log-rank test P =
      0.005). CONCLUSIONS: Patients with nonproteinuric diabetic kidney disease had
      better-controlled blood pressure and fewer typical morphological changes and were
      at lower risk of CKD progression and all-cause mortality.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Yamanouchi, Masayuki
AU  - Yamanouchi M
AUID- ORCID: http://orcid.org/0000-0003-3264-9691
AD  - Department of Nephrology and Laboratory Medicine, Faculty of Medicine, Institute 
      of Medical, Pharmaceutical and Health Sciences, Graduate School of Medical
      Sciences, Kanazawa University, Ishikawa, Japan m.yamanouchi@toranomon.gr.jp
      twada@m-kanazawa.jp.
AD  - Nephrology Center, Toranomon Hospital, Tokyo, Japan.
AD  - Nephrology Center, Toranomon Hospital Kajigaya, Kanagawa, Japan.
AD  - Okinaka Memorial Institute for Medical Research, Tokyo, Japan.
FAU - Furuichi, Kengo
AU  - Furuichi K
AD  - Division of Nephrology, Kanazawa University Hospital, Kanazawa, Japan.
FAU - Hoshino, Junichi
AU  - Hoshino J
AUID- ORCID: http://orcid.org/0000-0002-0444-101X
AD  - Nephrology Center, Toranomon Hospital, Tokyo, Japan.
AD  - Okinaka Memorial Institute for Medical Research, Tokyo, Japan.
FAU - Toyama, Tadashi
AU  - Toyama T
AD  - Division of Nephrology, Kanazawa University Hospital, Kanazawa, Japan.
FAU - Hara, Akinori
AU  - Hara A
AUID- ORCID: http://orcid.org/0000-0002-0399-1474
AD  - Division of Nephrology, Kanazawa University Hospital, Kanazawa, Japan.
FAU - Shimizu, Miho
AU  - Shimizu M
AUID- ORCID: http://orcid.org/0000-0002-7737-935X
AD  - Division of Nephrology, Kanazawa University Hospital, Kanazawa, Japan.
FAU - Kinowaki, Keiichi
AU  - Kinowaki K
AD  - Department of Pathology, Toranomon Hospital, Tokyo, Japan.
FAU - Fujii, Takeshi
AU  - Fujii T
AD  - Department of Pathology, Toranomon Hospital, Tokyo, Japan.
FAU - Ohashi, Kenichi
AU  - Ohashi K
AD  - Department of Pathology, Toranomon Hospital, Tokyo, Japan.
AD  - Department of Pathology, Yokohama City University Graduate School of Medicine,
      Kanagawa, Japan.
FAU - Yuzawa, Yukio
AU  - Yuzawa Y
AD  - Department of Nephrology, Fujita Health University School of Medicine, Aichi,
      Japan.
FAU - Kitamura, Hiroshi
AU  - Kitamura H
AD  - Department of Pathology, Clinical Research Center, National Hospital Organization
      Chiba-East National Hospital, Chiba, Japan.
FAU - Suzuki, Yoshiki
AU  - Suzuki Y
AD  - Health Administration Center, Niigata University, Niigata, Japan.
FAU - Sato, Hiroshi
AU  - Sato H
AD  - Clinical Pharmacology and Therapeutics, Tohoku University Graduate School of
      Pharmaceutical Sciences, Miyagi, Japan.
FAU - Uesugi, Noriko
AU  - Uesugi N
AD  - Department of Pathology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
FAU - Hisano, Satoshi
AU  - Hisano S
AD  - Department of Pathology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
FAU - Ueda, Yoshihiko
AU  - Ueda Y
AD  - Department of Pathology, Dokkyo Medical University Saitama Medical Center,
      Saitama, Japan.
FAU - Nishi, Shinichi
AU  - Nishi S
AD  - Division of Nephrology and Kidney Center, Kobe University Graduate School of
      Medicine, Hyogo, Japan.
FAU - Yokoyama, Hitoshi
AU  - Yokoyama H
AD  - Department of Nephrology, Kanazawa Medical University School of Medicine,
      Ishikawa, Japan.
FAU - Nishino, Tomoya
AU  - Nishino T
AD  - Department of Nephrology, Nagasaki University Hospital, Nagasaki, Japan.
FAU - Samejima, Kenichi
AU  - Samejima K
AUID- ORCID: http://orcid.org/0000-0001-8273-5155
AD  - Department of Nephrology, Nara Medical University, Nara, Japan.
FAU - Kohagura, Kentaro
AU  - Kohagura K
AD  - Department of Cardiovascular Medicine, Nephrology and Neurology, University of
      the Ryukyus School of Medicine, Okinawa, Japan.
FAU - Shibagaki, Yugo
AU  - Shibagaki Y
AD  - Division of Nephrology, Department of Internal Medicine, St. Marianna University 
      School of Medicine, Kanagawa, Japan.
FAU - Mise, Koki
AU  - Mise K
AUID- ORCID: http://orcid.org/0000-0003-0296-7429
AD  - Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama
      University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,
      Okayama, Japan.
FAU - Makino, Hirofumi
AU  - Makino H
AD  - Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama
      University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,
      Okayama, Japan.
FAU - Matsuo, Seiichi
AU  - Matsuo S
AD  - Division of Nephrology, Department of Internal Medicine, Nagoya University
      Graduate School of Medicine, Nagoya, Japan.
FAU - Ubara, Yoshifumi
AU  - Ubara Y
AD  - Nephrology Center, Toranomon Hospital Kajigaya, Kanagawa, Japan.
AD  - Okinaka Memorial Institute for Medical Research, Tokyo, Japan.
FAU - Wada, Takashi
AU  - Wada T
AUID- ORCID: http://orcid.org/0000-0002-0123-3645
CN  - Research Group of Diabetic Nephropathy, the Ministry of Health, Labour and
      Welfare, and the Japan Agency for Medical Research and Development
LA  - eng
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/06/19 00:00 [received]
PHST- 2019/02/04 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - dc18-1320 [pii]
AID - 10.2337/dc18-1320 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Mar 4. pii: dc18-1320. doi: 10.2337/dc18-1320.

PMID- 30833371
OWN - NLM
STAT- Publisher
LR  - 20190306
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Mar 4
TI  - Improved Time in Range and Glycemic Variability With Sotagliflozin in Combination
      With Insulin in Adults With Type 1 Diabetes: A Pooled Analysis of 24-Week
      Continuous Glucose Monitoring Data From the inTandem Program.
LID - dc182149 [pii]
LID - 10.2337/dc18-2149 [doi]
AB  - OBJECTIVE: To evaluate effects of the dual sodium-glucose cotransporter (SGLT) 1 
      and SGLT2 inhibitor sotagliflozin in combination with insulin on glucose time in 
      range (TIR) and glucose excursions, postprandial glucose (PPG), and other
      glycemic metrics in adults with type 1 diabetes using masked continuous glucose
      monitoring (CGM). RESEARCH DESIGN AND METHODS: Data sets from the inTandem1
      (clinical trial reg. no. NCT02384941) and inTandem2 (clinical trial reg. no.
      NCT02421510) double-blind randomized trials evaluating sotagliflozin versus
      placebo in adults with type 1 diabetes treated with optimized insulin were pooled
      for analyses of masked CGM data from a subset of participants in each trial. The 
      pooled cohort included patients randomized to receive placebo (n = 93),
      sotagliflozin 200 mg (n = 89), or sotagliflozin 400 mg (n = 96). The primary
      outcome was change from baseline to week 24 in glucose TIR (3.9-10.0 mmol/L
      [70-180 mg/dL]). Secondary end points included time below and above the target
      range and 2-h PPG level assessed after a standardized mixed meal. RESULTS: Mean
      percentage of glucose TIR/percentage time spent at <3.9 mmol/L (<70 mg/dL) during
      week 24 was 51.6%/5.9%, 57.8%/5.5%, and 64.2%/5.5%, with placebo, sotagliflozin
      200 mg, and sotagliflozin 400 mg, respectively, which corresponded to a
      placebo-adjusted change from a baseline of +5.4/-0.3% (P = 0.026; +1.3/-0.1
      h/day) for sotagliflozin 200 mg and +11.7/-0.1% (P < 0.001; +2.8/-0.02 h/day) for
      sotagliflozin 400 mg. Placebo-adjusted PPG reductions were 1.9 +/- 0.7 mmol/L (35
      +/- 13 mg/dL; P = 0.004) and 2.8 +/- 0.7 mmol/L (50 +/- 13 mg/dL; P < 0.001) with
      sotagliflozin 200 and 400 mg, respectively. CONCLUSIONS: Combined with optimized 
      insulin in type 1 diabetes, sotagliflozin significantly increased glucose TIR
      without increasing time spent at <3.9 mmol/L and reduced PPG, thereby improving
      glycemic control.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Danne, Thomas
AU  - Danne T
AUID- ORCID: http://orcid.org/0000-0003-0773-6961
AD  - Department of Diabetes, Endocrinology, and Clinical Research, Childrens and Youth
      Hospital Auf der Bult, Hannover Medical School, Hannover, Germany danne@hka.de.
FAU - Cariou, Bertrand
AU  - Cariou B
AUID- ORCID: http://orcid.org/0000-0002-1580-8040
AD  - L'institut du thorax, Department of Endocrinology, CIC 1413 INSERM, CHU Nantes,
      Nantes, France.
FAU - Buse, John B
AU  - Buse JB
AUID- ORCID: http://orcid.org/0000-0002-9723-3876
AD  - Department of Medicine, University of North Carolina School of Medicine, Chapel
      Hill, NC.
FAU - Garg, Satish K
AU  - Garg SK
AD  - Department of Medicine and Pediatrics, Barbara Davis Center for Diabetes,
      University of Colorado Denver, Aurora, CO.
FAU - Rosenstock, Julio
AU  - Rosenstock J
AUID- ORCID: http://orcid.org/0000-0001-8324-3275
AD  - Dallas Diabetes Research Center at Medical City, Dallas, TX.
FAU - Banks, Phillip
AU  - Banks P
AD  - Lexicon Pharmaceuticals, Inc., The Woodlands, TX.
FAU - Kushner, Jake A
AU  - Kushner JA
AUID- ORCID: http://orcid.org/0000-0002-3646-1744
AD  - Department of Pediatrics, Baylor College of Medicine and Texas Children's
      Hospital, Houston, TX.
FAU - McGuire, Darren K
AU  - McGuire DK
AUID- ORCID: http://orcid.org/0000-0002-6412-7989
AD  - Department of Internal Medicine, Division of Cardiology, University of Texas
      Southwestern Medical Center, Dallas, TX.
FAU - Peters, Anne L
AU  - Peters AL
AD  - Keck School of Medicine of the University of Southern California, Los Angeles,
      CA.
FAU - Sawhney, Sangeeta
AU  - Sawhney S
AD  - Lexicon Pharmaceuticals, Inc., The Woodlands, TX.
FAU - Strumph, Paul
AU  - Strumph P
AD  - Lexicon Pharmaceuticals, Inc., The Woodlands, TX.
LA  - eng
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/10/12 00:00 [received]
PHST- 2019/01/27 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - dc18-2149 [pii]
AID - 10.2337/dc18-2149 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Mar 4. pii: dc18-2149. doi: 10.2337/dc18-2149.

PMID- 30833370
OWN - NLM
STAT- Publisher
LR  - 20190305
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Mar 4
TI  - Risk Factors for Kidney Disease in Type 1 Diabetes.
LID - dc182062 [pii]
LID - 10.2337/dc18-2062 [doi]
AB  - OBJECTIVE: In type 1 diabetes (T1D), the course of microalbuminuria is
      unpredictable and timing of glomerular filtration rate (GFR) loss is uncertain.
      Thus, there is a need to identify the risk factors associated with the
      development of more advanced stages of kidney disease through large, long-term
      systematic analysis. RESEARCH DESIGN AND METHODS: Multivariable Cox proportional 
      hazards models assessed the association of baseline and time-dependent glycemic
      and nonglycemic risk factors for incident macroalbuminuria and reduced estimated 
      GFR (eGFR; defined as <60 mL/min/1.73 m(2)) over a mean of 27 years in the
      Diabetes Control and Complications Trial (DCCT) cohort. RESULTS: Higher mean
      HbA1c (hazard ratio [HR] 1.969 per 1% higher level [95% CI 1.671-2.319]) and male
      sex (HR 2.767 [95% CI 1.951-3.923]) were the most significant factors
      independently associated with incident macroalbuminuria, whereas higher mean
      triglycerides, higher pulse, higher systolic blood pressure (BP), longer diabetes
      duration, higher current HbA1c, and lower mean weight had lower magnitude
      associations. For incident reduced eGFR, higher mean HbA1c (HR 1.952 per 1%
      higher level [95% CI 1.714-2.223]) followed by higher mean triglycerides, older
      age, and higher systolic BP were the most significant factors. CONCLUSIONS:
      Although several risk factors associated with macroalbuminuria and reduced eGFR
      were identified, higher mean glycemic exposure was the strongest determinant of
      kidney disease among the modifiable risk factors. These findings may inform
      targeted clinical strategies for the frequency of screening, prevention, and
      treatment of kidney disease in T1D.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Perkins, Bruce A
AU  - Perkins BA
AUID- ORCID: http://orcid.org/0000-0002-5885-0046
AD  - Endocrinology and Metabolism, University of Toronto, Toronto, Canada.
FAU - Bebu, Ionut
AU  - Bebu I
AUID- ORCID: http://orcid.org/0000-0002-4944-7968
AD  - Biostatistics Center, The George Washington University, Rockville, MD.
FAU - de Boer, Ian H
AU  - de Boer IH
AUID- ORCID: http://orcid.org/0000-0003-1571-7592
AD  - Division of Nephrology, University of Washington, Seattle, WA.
FAU - Molitch, Mark
AU  - Molitch M
AUID- ORCID: http://orcid.org/0000-0002-8492-3587
AD  - Endocrinology, Metabolism, and Molecular Medicine, Northwestern University,
      Chicago, IL.
FAU - Tamborlane, William
AU  - Tamborlane W
AD  - Pediatrics and Endocrinology, Yale School of Medicine, New Haven, CT.
FAU - Lorenzi, Gayle
AU  - Lorenzi G
AD  - University of California, San Diego, CA.
FAU - Herman, William
AU  - Herman W
AUID- ORCID: http://orcid.org/0000-0002-0502-674X
AD  - Internal Medicine/MEND, University of Michigan Medical Center, Ann Arbor, MI.
FAU - White, Neil H
AU  - White NH
AD  - Pediatrics, Washington University, St. Louis, MO.
FAU - Pop-Busui, Rodica
AU  - Pop-Busui R
AUID- ORCID: http://orcid.org/0000-0002-2042-1350
AD  - Metabolism, Endocrinology, and Diabetes, University of Michigan, Ann Arbor, MI.
FAU - Paterson, Andrew D
AU  - Paterson AD
AUID- ORCID: http://orcid.org/0000-0002-9169-118X
AD  - Genetics and Genomic Biology, Hospital for Sick Children, Toronto, Canada.
FAU - Orchard, Trevor
AU  - Orchard T
AD  - Epidemiology, University of Pittsburgh, Pittsburgh, PA.
FAU - Cowie, Catherine
AU  - Cowie C
AD  - National Institute of Diabetes and Digestive and Kidney Diseases/National
      Insitutes of Health, Bethesda, MD.
FAU - Lachin, John M
AU  - Lachin JM
AUID- ORCID: http://orcid.org/0000-0001-9838-2841
AD  - Biostatistics Center, The George Washington University, Rockville, MD
      jml@bsc.gwu.edu.
CN  - Diabetes Control and Complications Trial (DCCT)-Epidemiology of Diabetes
      Interventions and Complications (EDIC) Research Group
LA  - eng
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/10/01 00:00 [received]
PHST- 2019/02/03 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - dc18-2062 [pii]
AID - 10.2337/dc18-2062 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Mar 4. pii: dc18-2062. doi: 10.2337/dc18-2062.

PMID- 30833368
OWN - NLM
STAT- Publisher
LR  - 20190305
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Mar 4
TI  - Risk Factors for Retinopathy in Type 1 Diabetes: The DCCT/EDIC Study.
LID - dc182308 [pii]
LID - 10.2337/dc18-2308 [doi]
AB  - OBJECTIVE: The Diabetes Control and Complications Trial (DCCT) demonstrated that 
      intensive therapy reduced the development and progression of retinopathy in type 
      1 diabetes (T1D) compared with conventional therapy. The Epidemiology of Diabetes
      Interventions and Complications (EDIC) study observational follow-up showed
      persistent benefits. In addition to glycemia, we now examine other potential
      retinopathy risk factors (modifiable and nonmodifiable) over more than 30 years
      of follow-up in DCCT/EDIC. RESEARCH DESIGN AND METHODS: The retinopathy outcomes 
      were proliferative diabetic retinopathy (PDR), clinically significant macular
      edema (CSME), and ocular surgery. The survival (event-free) probability was
      estimated using the Kaplan-Meier method. Cox proportional hazards models assessed
      the association between risk factors and subsequent risk of retinopathy. Both
      forward- and backward-selection approaches determined the multivariable models.
      RESULTS: Rate of ocular events per 1,000 person-years was 12 for PDR, 14.5 for
      CSME, and 7.6 for ocular surgeries. Approximately 65%, 60%, and 70% of
      participants remained free of PDR, CSME, and ocular surgery, respectively. The
      greatest risk factors for PDR in descending order were higher mean HbA1c, longer 
      duration of T1D, elevated albumin excretion rate (AER), and higher mean diastolic
      blood pressure (DBP). For CSME, risk factors, in descending order, were higher
      mean HbA1c, longer duration of T1D, and greater age and DBP, and for ocular
      surgeries were higher mean HbA1c, older age, and longer duration of T1D.
      CONCLUSIONS: Mean HbA1c was the strongest risk factor for the progression of
      retinopathy. Although glycemic control is important, elevated AER and DBP were
      other modifiable risk factors associated with the progression of retinopathy.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Hainsworth, Dean P
AU  - Hainsworth DP
AD  - Mason Eye Institute, University of Missouri, Columbia, MO.
FAU - Bebu, Ionut
AU  - Bebu I
AUID- ORCID: http://orcid.org/0000-0002-4944-7968
AD  - Biostatistics Center, The George Washington University, Washington, DC.
FAU - Aiello, Lloyd P
AU  - Aiello LP
AD  - Department of Ophthalmology, Joslin Diabetes Center, Boston, MA.
FAU - Sivitz, William
AU  - Sivitz W
AD  - Department of Internal Medicine, University of Iowa, Iowa City, IA.
FAU - Gubitosi-Klug, Rose
AU  - Gubitosi-Klug R
AUID- ORCID: http://orcid.org/0000-0002-7376-6870
AD  - Rainbow Babies and Children's Hospital, Cleveland, OH.
FAU - Malone, John
AU  - Malone J
AD  - Diabetes Center, University of South Florida, Tampa, FL.
FAU - White, Neil H
AU  - White NH
AD  - Pediatrics, Washington University, St. Louis, MO.
FAU - Danis, Ronald
AU  - Danis R
AD  - University of Wisconsin, Madison, WI.
FAU - Wallia, Amisha
AU  - Wallia A
AUID- ORCID: http://orcid.org/0000-0002-3183-4062
AD  - Department of Medicine, Northwestern University, Evanston, IL.
FAU - Gao, Xiaoyu
AU  - Gao X
AD  - Biostatistics Center, The George Washington University, Washington, DC.
FAU - Barkmeier, Andrew J
AU  - Barkmeier AJ
AD  - University of New Mexico, Albuquerque, NM.
FAU - Das, Arup
AU  - Das A
AD  - University of New Mexico, Albuquerque, NM.
FAU - Patel, Shriji
AU  - Patel S
AD  - Vanderbilt University Medical Center, Nashville, TN.
FAU - Gardner, Thomas W
AU  - Gardner TW
AD  - University of Michigan Kellogg Eye Center, Ann Arbor, MI.
FAU - Lachin, John M
AU  - Lachin JM
AUID- ORCID: http://orcid.org/0000-0001-9838-2841
AD  - Biostatistics Center, The George Washington University, Washington, DC
      jml@bsc.gwu.edu.
CN  - Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes
      Interventions and Complications (EDIC) Research Group
LA  - eng
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/11/05 00:00 [received]
PHST- 2019/01/24 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - dc18-2308 [pii]
AID - 10.2337/dc18-2308 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Mar 4. pii: dc18-2308. doi: 10.2337/dc18-2308.

PMID- 30833367
OWN - NLM
STAT- Publisher
LR  - 20190305
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
DP  - 2019 Mar 4
TI  - Randomized Trial of a Tailored Cognitive Behavioral Intervention in Type 2
      Diabetes With Comorbid Depressive and/or Regimen-Related Distress Symptoms:
      12-Month Outcomes From COMRADE.
LID - dc181841 [pii]
LID - 10.2337/dc18-1841 [doi]
AB  - OBJECTIVE: This study evaluated the effect of cognitive behavioral therapy (CBT) 
      plus lifestyle counseling in primary care on hemoglobin A1c (HbA1c) in rural
      adult patients with type 2 diabetes (T2D) and comorbid depressive or
      regimen-related distress (RRD) symptoms. RESEARCH DESIGN AND METHODS: This study 
      was a randomized controlled trial of a 16-session severity-tailored CBT plus
      lifestyle counseling intervention compared with usual care. Outcomes included
      changes in HbA1c, RRD, depressive symptoms, self-care behaviors, and medication
      adherence across 12 months. RESULTS: Patients included 139 diverse, rural adults 
      (mean age 52.6 +/- 9.5 years; 72% black; BMI 37.0 +/- 9.0) with T2D (mean HbA1c =
      9.6 [81 mmol/mol] +/- 2.0) and comorbid depressive or distress symptoms. Using
      intent-to-treat analyses, patients in the intervention experienced marginally
      significant improvements in HbA1c (-0.92 +/- 1.81 vs. -0.31 +/- 2.04; P = 0.06)
      compared with usual care. However, intervention patients experienced
      significantly greater improvements in RRD (-1.12 +/- 1.05 vs. -0.31 +/- 1.22; P =
      0.001), depressive symptoms (-3.39 +/- 5.00 vs. -0.90 +/- 6.17; P = 0.01),
      self-care behaviors (+1.10 +/- 1.30 vs. +0.58 +/- 1.45; P = 0.03), and medication
      adherence (+1.00 +/- 2.0 vs. +0.17 +/- 1.0; P = 0.02) versus usual care.
      Improvement in HbA1c correlated with improvement in RRD (r = 0.3; P = 0.0001) and
      adherence (r = -0.23; P = 0.007). CONCLUSIONS: Tailored CBT with lifestyle
      counseling improves behavioral outcomes and may improve HbA1c in rural patients
      with T2D and comorbid depressive and/or RRD symptoms.
CI  - (c) 2019 by the American Diabetes Association.
FAU - Cummings, Doyle M
AU  - Cummings DM
AUID- ORCID: http://orcid.org/0000-0002-8237-7885
AD  - Department of Family Medicine, Brody School of Medicine, East Carolina
      University, Greenville, NC cummingsd@ecu.edu.
AD  - Center for Health Disparities, East Carolina University, Greenville, NC.
FAU - Lutes, Lesley D
AU  - Lutes LD
AD  - Department of Psychology, University of British Columbia, Kelowna, British
      Columbia, Canada.
FAU - Littlewood, Kerry
AU  - Littlewood K
AD  - School of Social Work, University of South Florida, Tampa, FL.
FAU - Solar, Chelsey
AU  - Solar C
AD  - Department of Psychology, East Carolina University, Greenville, NC.
FAU - Carraway, Marissa
AU  - Carraway M
AD  - Department of Family Medicine, Brody School of Medicine, East Carolina
      University, Greenville, NC.
FAU - Kirian, Kari
AU  - Kirian K
AD  - Department of Family Medicine, Brody School of Medicine, East Carolina
      University, Greenville, NC.
FAU - Patil, Shivajirao
AU  - Patil S
AD  - Department of Family Medicine, Brody School of Medicine, East Carolina
      University, Greenville, NC.
FAU - Adams, Alyssa
AU  - Adams A
AD  - Department of Family Medicine, Brody School of Medicine, East Carolina
      University, Greenville, NC.
FAU - Ciszewski, Stefanie
AU  - Ciszewski S
AD  - Department of Psychology, University of British Columbia, Kelowna, British
      Columbia, Canada.
FAU - Edwards, Sheila
AU  - Edwards S
AD  - Department of Family Medicine, Brody School of Medicine, East Carolina
      University, Greenville, NC.
FAU - Gatlin, Peggy
AU  - Gatlin P
AD  - Department of Family Medicine, Brody School of Medicine, East Carolina
      University, Greenville, NC.
FAU - Hambidge, Bertha
AU  - Hambidge B
AD  - Department of Family Medicine, Brody School of Medicine, East Carolina
      University, Greenville, NC.
LA  - eng
PT  - Journal Article
DEP - 20190304
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/08/31 00:00 [received]
PHST- 2019/02/04 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - dc18-1841 [pii]
AID - 10.2337/dc18-1841 [doi]
PST - aheadofprint
SO  - Diabetes Care. 2019 Mar 4. pii: dc18-1841. doi: 10.2337/dc18-1841.

PMID- 30848827
OWN - NLM
STAT- Publisher
LR  - 20190308
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Mar 8
TI  - Plasma Fibroblast Growth Factor 21 is Associated with Severity of Nonalcoholic
      Steatohepatitis in Patients with Obesity and Type 2 Diabetes.
LID - jc.2018-02414 [pii]
LID - 10.1210/jc.2018-02414 [doi]
AB  - CONTEXT: The relationship between plasma FGF21, insulin resistance and
      steatohepatitis has not been systematically assessed. OBJECTIVE: To determine if 
      higher plasma FGF21 is associated with worse steatohepatitis on liver biopsy in
      patients with NAFLD. DESIGN AND SETTING: Cross-sectional study in a University
      Hospital.Patients Interventions and Main Outcome MeasuresPatients with BMI>25
      (n=187) underwent: (a) euglycemic hyperinsulinemic clamp to assess tissue
      specific insulin resistance; (b) liver magnetic resonance spectroscopy (1H-MRS)
      for intrahepatic triglyceride (IHTG) quantification, (c) liver biopsy (if NAFLD
      present; n=146); and (d) fasting plasma FGF21 levels. METHODS AND RESULTS:
      Patients were divided into three groups: (a) No NAFLD (n=41); (b) No NASH:
      patients with isolated steatosis or borderline NASH (n=52); and (c) NASH:
      patients with definite NASH (n=94). Groups were well-matched for age/gender,
      prevalence of T2DM and A1c.During euglycemic hyperinsulinemic insulin clamp,
      insulin sensitivity in skeletal muscle and adipose tissue worsened from No NAFLD 
      to NASH (both p<0.001). Plasma FGF21 levels correlated inversely with insulin
      sensitivity in adipose tissue (r=-0.17, p=0.006) and skeletal muscle (r=-0.23,
      p=0.007), but not with liver insulin sensitivity. Plasma FGF21 was higher in
      patients with NASH (453+/-262 pg/ml) when compared to No NASH (341+/-198pg/ml,
      p=0.03) or No NAFLD (325+/-289 pg/ml, p=0.02). Plasma FGF21 increased with the
      severity of necroinflammation (p=0.02), and most significantly with worse
      fibrosis (p<0.001), but not with worsening steatosis (p=0.60). CONCLUSIONS:
      Plasma FGF21 correlates with severity of steatohepatitis, in particular of
      fibrosis, in patients with NASH. Measurement of FGF21 may help identify patients 
      at the highest risk of disease progression.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Barb, Diana
AU  - Barb D
AD  - Division of Endocrinology, Diabetes and Metabolism, Department of Medicine,
      University of Florida College of Medicine, Gainesville, FL.
FAU - Bril, Fernando
AU  - Bril F
AD  - Division of Endocrinology, Diabetes and Metabolism, Department of Medicine,
      University of Florida College of Medicine, Gainesville, FL.
FAU - Kalavalapalli, Srilaxmi
AU  - Kalavalapalli S
AD  - Division of Endocrinology, Diabetes and Metabolism, Department of Medicine,
      University of Florida College of Medicine, Gainesville, FL.
FAU - Cusi, Kenneth
AU  - Cusi K
AD  - Division of Endocrinology, Diabetes and Metabolism, Department of Medicine,
      University of Florida College of Medicine, Gainesville, FL.
AD  - Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine,
      Malcom Randall Veterans Affairs Medical Center, Gainesville, Florida.
LA  - eng
PT  - Journal Article
DEP - 20190308
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/03/09 06:00
MHDA- 2019/03/09 06:00
CRDT- 2019/03/09 06:00
PHST- 2018/11/07 00:00 [received]
PHST- 2019/03/04 00:00 [accepted]
PHST- 2019/03/09 06:00 [entrez]
PHST- 2019/03/09 06:00 [pubmed]
PHST- 2019/03/09 06:00 [medline]
AID - 5371245 [pii]
AID - 10.1210/jc.2018-02414 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Mar 8. pii: 5371245. doi: 10.1210/jc.2018-02414.

PMID- 30848792
OWN - NLM
STAT- Publisher
LR  - 20190308
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Mar 8
TI  - Skeletal Fragility & Its Clinical Determinants In Children With Type 1 Diabetes.
LID - jc.2019-00084 [pii]
LID - 10.1210/jc.2019-00084 [doi]
AB  - CONTEXT: Type 1 diabetes (T1D) is associated with an increased fracture risk at
      all ages. OBJECTIVE: To understand the determinants of bone health and fractures 
      in children with T1D. DESIGN: Case-control study of children with T1D on bone
      turnover markers, DXA and 3T-MRI of the proximal tibia to assess bone
      microarchitecture and vertebral marrow adiposity, compared to age and sex-matched
      healthy children. RESULTS: 32 children with T1D at a median (range) age of 13.7
      years (10.4,16.7) and 26 controls aged 13.8 years (10.2,17.8) were recruited. In 
      children with T1D, serum BAP SDS, CTX SDS, and total body and lumbar spine BMD
      SDS were lower (all p<0.05). Children with T1D also had lower trabecular volume
      [0.55 (0.47,0.63) vs 0.59 (0.47,0.63); p=0.024], lower trabecular number [1.67
      (1.56,1.93) vs 1.82 (1.56,1.99); p=0.004] and higher trabecular separation [0.27 
      (0.21,0.32) vs 0.24 (0.20,0.33); p=0.001] than controls. Marrow adiposity was
      similar in both groups (p=0.25). Bone formation as assessed by BAP was lower in
      children with poorer glycemic control (p=0.009) and who were acidotic at initial 
      presentation (p=0.017) but higher in children on continuous subcutaneous insulin 
      infusion (p=0.025). Fractures were more likely to be encountered in children with
      T1D compared to controls [31% vs 19%; p<0.001]. Compared to those without
      fractures, the T1D children with a fracture history had poorer glycemic control
      (p=0.007) and lower total body BMD (p<0.001) but no differences in bone
      microarchitecture. CONCLUSION: Children with T1D display a low bone turnover
      state with reduced bone mineralisation and poorer bone microarchitecture.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Chen, Suet Ching
AU  - Chen SC
AD  - Developmental Endocrinology Research Group, School of Medicine, Dentistry &
      Nursing, University of Glasgow, UK.
AD  - Paediatric Diabetes Service, NHS Greater Glasgow & Clyde, Glasgow, UK.
FAU - Shepherd, Sheila
AU  - Shepherd S
AD  - Developmental Endocrinology Research Group, School of Medicine, Dentistry &
      Nursing, University of Glasgow, UK.
FAU - McMillan, Martin
AU  - McMillan M
AD  - Developmental Endocrinology Research Group, School of Medicine, Dentistry &
      Nursing, University of Glasgow, UK.
FAU - McNeilly, Jane
AU  - McNeilly J
AD  - Department of Clinical Biochemistry, Royal Hospital for Children, NHS Greater
      Glasgow and Clyde, Glasgow UK.
FAU - Foster, John
AU  - Foster J
AD  - Department of Clinical Physics, NHS Greater Glasgow and Clyde, Glasgow UK.
FAU - Wong, Sze Choong
AU  - Wong SC
AD  - Developmental Endocrinology Research Group, School of Medicine, Dentistry &
      Nursing, University of Glasgow, UK.
FAU - Robertson, Kenneth J
AU  - Robertson KJ
AD  - Paediatric Diabetes Service, NHS Greater Glasgow & Clyde, Glasgow, UK.
FAU - Ahmed, S Faisal
AU  - Ahmed SF
AD  - Developmental Endocrinology Research Group, School of Medicine, Dentistry &
      Nursing, University of Glasgow, UK.
LA  - eng
PT  - Journal Article
DEP - 20190308
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/03/09 06:00
MHDA- 2019/03/09 06:00
CRDT- 2019/03/09 06:00
PHST- 2019/01/11 00:00 [received]
PHST- 2019/03/04 00:00 [accepted]
PHST- 2019/03/09 06:00 [entrez]
PHST- 2019/03/09 06:00 [pubmed]
PHST- 2019/03/09 06:00 [medline]
AID - 5371250 [pii]
AID - 10.1210/jc.2019-00084 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Mar 8. pii: 5371250. doi: 10.1210/jc.2019-00084.

PMID- 30848791
OWN - NLM
STAT- Publisher
LR  - 20190308
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Mar 8
TI  - Separate and Combined Effects of GIP and GLP-1 Infusions on Bone Metabolism in
      Overweight Men without Diabetes.
LID - jc.2019-00008 [pii]
LID - 10.1210/jc.2019-00008 [doi]
AB  - CONTEXT: The gut-derived incretin hormones, glucose-dependent insulinotropic
      polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), have been suggested to
      play a role in bone metabolism. Exogenous administration of GIP inhibits bone
      resorption, while the effect of GLP-1 is less clear. Furthermore, the combined
      effect of exogenous GIP and GLP-1 on bone metabolism is unknown. OBJECTIVE: To
      investigate the effect of separate and combined infusions of the incretin
      hormones GIP and GLP-1 on bone resorption and formation. DESIGN: Randomized,
      double-blinded, placebo-controlled, crossover study including five study days.
      PARTICIPANTS: Seventeen overweight/obese men. INTERVENTIONS: On the first study
      day, a 50 g oral glucose tolerance test (OGTT) was performed. On the next four
      study days, isoglycemic IV glucose infusions (IIGI), mimicking the glucose
      excursions from the OGTT, were performed with concomitant infusions of GIP (4
      pmol/kg/min), GLP-1 (1 pmol/kg/min), GIP+GLP-1 (4 and 1 pmol/kg/min,
      respectively) or placebo, respectively. PRIMARY OUTCOMES: Changes in bone
      resorption assessed by measurements of carboxy-terminal type I collagen
      crosslinks (CTX), and in bone formation as assessed by procollagen type 1
      N-terminal propeptide (P1NP) concentrations. RESULTS: During the OGTT, CTX was
      significantly lowered by 54+/-13% from baseline (mean+/-SD) compared to 28+/-12% 
      during IIGI+saline (P <0.0001). During IIGI+GLP-1 and IIGI+GIP, respectively, CTX
      was lowered by 65+/-16% and 74+/-9% from baseline, while IGII+GIP+GLP-1 lowered
      CTX by 84+/-4% from baseline. P1NP levels were unaffected by the interventions.
      CONCLUSIONS: Our data suggest that GLP-1, like GIP, may be involved in regulation
      of bone resorption and that GIP and GLP-1 together have partially additive
      inhibitory effects.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Bergmann, Natasha Chidekel
AU  - Bergmann NC
AD  - Clinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte
      Hospital, Hellerup, Denmark.
AD  - Department of In Vivo Pharmacology, Zealand Pharma A/S, Glostrup, Denmark.
AD  - Department of Biomedical Sciences, Faculty of Health and Medical Sciences,
      University of Copenhagen, Copenhagen, Denmark.
FAU - Lund, Asger
AU  - Lund A
AD  - Clinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte
      Hospital, Hellerup, Denmark.
AD  - Department of Medicine, Gentofte Hospital, Hellerup, Denmark.
FAU - Gasbjerg, Laerke Smidt
AU  - Gasbjerg LS
AD  - Clinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte
      Hospital, Hellerup, Denmark.
AD  - Department of Biomedical Sciences, 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 - Jorgensen, Niklas Rye
AU  - Jorgensen NR
AD  - Department of Clinical Chemistry, Rigshospitalet, University of Copenhagen,
      Glostrup, Denmark.
AD  - OPEN, Odense University Hospital, Odense, Denmark.
FAU - Jessen, Lene
AU  - Jessen L
AD  - Department of In Vivo Pharmacology, Zealand Pharma A/S, Glostrup, Denmark.
FAU - Hartmann, Bolette
AU  - Hartmann B
AD  - Department of Biomedical Sciences, 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 - Holst, Jens Juul
AU  - Holst JJ
AD  - Department of Biomedical Sciences, 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 - Christensen, Mikkel Bring
AU  - Christensen MB
AD  - Clinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte
      Hospital, Hellerup, Denmark.
AD  - Department of Clinical Medicine, Faculty of Health and Medical Sciences,
      University of Copenhagen, Copenhagen, Denmark.
AD  - Department of Clinical Pharmacology, Bispebjerg Hospital, Copenhagen, Denmark.
FAU - Vilsboll, Tina
AU  - Vilsboll T
AD  - Clinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte
      Hospital, Hellerup, Denmark.
AD  - Department of Clinical Medicine, Faculty of Health and Medical Sciences,
      University of Copenhagen, Copenhagen, Denmark.
FAU - Knop, Filip Krag
AU  - Knop FK
AD  - Clinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte
      Hospital, Hellerup, Denmark.
AD  - Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health
      and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
AD  - Department of Clinical Medicine, Faculty of Health and Medical Sciences,
      University of Copenhagen, Copenhagen, Denmark.
LA  - eng
PT  - Journal Article
DEP - 20190308
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/03/09 06:00
MHDA- 2019/03/09 06:00
CRDT- 2019/03/09 06:00
PHST- 2019/01/03 00:00 [received]
PHST- 2019/03/04 00:00 [accepted]
PHST- 2019/03/09 06:00 [entrez]
PHST- 2019/03/09 06:00 [pubmed]
PHST- 2019/03/09 06:00 [medline]
AID - 5371246 [pii]
AID - 10.1210/jc.2019-00008 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Mar 8. pii: 5371246. doi: 10.1210/jc.2019-00008.

PMID- 30844073
OWN - NLM
STAT- Publisher
LR  - 20190329
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Mar 7
TI  - Continuous Glucose Monitoring Predicts Progression to Diabetes in Autoantibody
      Positive Children.
LID - jc.2018-02196 [pii]
LID - 10.1210/jc.2018-02196 [doi]
AB  - CONTEXT: Accurate measures are needed for the prediction and diagnosis of type 1 
      diabetes (T1D) in at risk subjects. OBJECTIVE: The purpose of this study was to
      explore the value of continuous glucose monitoring (CGM) in predicting T1D onset.
      DESIGN AND SETTING: The Diabetes Autoimmunity Study in the Young (DAISY)
      prospectively follows children at increased risk for development of islet
      autoantibodies (Ab+) and T1D. PARTICIPANTS: We analyzed 23 Ab+ subjects with
      available longitudinal CGM data. MAIN OUTCOME MEASURE: CGM metrics as glycemic
      predictors of progression to diabetes. RESULTS: Of 23 Ab+ subjects with a
      baseline CGM, eight progressed to diabetes at a median age of 13.8 years during a
      median follow-up of 17.7 years (IQR 14.6-22.0 years). Compared to
      non-progressors, subjects who progressed to diabetes had significantly increased 
      baseline glycemic variability (SD 29 vs 21 mg/dl, p=0.047), daytime sensor
      average (122 vs 106 mg/dl, p=0.02), and daytime sensor area under the curve (AUC,
      470,370 vs 415,465, p=0.047). They spent 24% of time above 140 mg/dl and 12%
      above 160 mg/dl compared to, respectively, 8% and 3% for non-progressors (both
      p=0.005). A receiver-operating curve (ROC) analysis showed AUC of 0.85 for %time 
      spent above 140 or 160 mg/dl. The cutoff of 18% time spent above 140 mg/dl had
      75% sensitivity, 100% specificity, and 100% PPV for diabetes prediction, although
      these values could change as some non-progressors may develop diabetes with
      longer follow-up. CONCLUSIONS: In conclusion, >18% CGM time spent above 140 mg/dl
      predicts progression to diabetes in islet Ab+ children.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Steck, Andrea K
AU  - Steck AK
AD  - Barbara Davis Center for Childhood Diabetes, University of Colorado School of
      Medicine, Aurora, Colorado, USA.
FAU - Dong, Fran
AU  - Dong F
AD  - Barbara Davis Center for Childhood Diabetes, University of Colorado School of
      Medicine, Aurora, Colorado, USA.
FAU - Taki, Iman
AU  - Taki I
AD  - Barbara Davis Center for Childhood Diabetes, University of Colorado School of
      Medicine, Aurora, Colorado, USA.
FAU - Hoffman, Michelle
AU  - Hoffman M
AD  - Barbara Davis Center for Childhood Diabetes, University of Colorado School of
      Medicine, Aurora, Colorado, USA.
FAU - Simmons, Kimber
AU  - Simmons K
AD  - Barbara Davis Center for Childhood Diabetes, University of Colorado School of
      Medicine, Aurora, Colorado, USA.
FAU - Frohnert, Brigitte I
AU  - Frohnert BI
AD  - Barbara Davis Center for Childhood Diabetes, University of Colorado School of
      Medicine, Aurora, Colorado, USA.
FAU - Rewers, Marian J
AU  - Rewers MJ
AD  - Barbara Davis Center for Childhood Diabetes, University of Colorado School of
      Medicine, Aurora, Colorado, USA.
LA  - eng
GR  - R01 DK032493/DK/NIDDK NIH HHS/United States
GR  - R37 DK032493/DK/NIDDK NIH HHS/United States
PT  - Journal Article
DEP - 20190307
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/03/08 06:00
MHDA- 2019/03/08 06:00
CRDT- 2019/03/08 06:00
PHST- 2018/10/10 00:00 [received]
PHST- 2019/03/01 00:00 [accepted]
PHST- 2019/03/08 06:00 [entrez]
PHST- 2019/03/08 06:00 [pubmed]
PHST- 2019/03/08 06:00 [medline]
AID - 5370167 [pii]
AID - 10.1210/jc.2018-02196 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Mar 7. pii: 5370167. doi: 10.1210/jc.2018-02196.

PMID- 30835282
OWN - NLM
STAT- Publisher
LR  - 20190305
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
DP  - 2019 Mar 5
TI  - Gestational diabetes, but not pre-pregnancy overweight predicts cardio-metabolic 
      markers in offspring twenty years later.
LID - jc.2018-02743 [pii]
LID - 10.1210/jc.2018-02743 [doi]
AB  - CONTEXT: Maternal gestational diabetes (GDM) and pre-pregnancy overweight/obesity
      (body mass index, BMI >/=25kg/m2) may adversely affect offspring cardio-metabolic
      health. OBJECTIVE: To assess associations of maternal GDM and pre-pregnancy
      overweight/obesity with adult offspring cardio-metabolic risk factors. DESIGN:
      Longitudinal cohort study (ESTER and AYLS). SETTING: Province of Uusimaa and
      Northern Finland. PARTICIPANTS: At mean age 24.1 years (SD 1.3), we classified
      offspring to offspring of mothers with 1) GDM regardless of pre-pregnancy BMI
      (OGDM; n=193), 2) normoglycemic mothers with pre-pregnancy overweight/obesity
      (ONO, n=157) and 3) normoglycemic mothers with pre-pregnancy BMI<25kg/m2
      (controls, n=556). MAIN OUTCOME MEASURES: We assessed cardio-metabolic biomarkers
      from blood and measured resting blood pressure and heart rate. RESULTS: Compared 
      with controls, OGDM and ONO had higher fasting glucose [1.6% (95% confidence
      interval 0.1, 3.1)]; [2.3% (0.5, 4.3), respectively]; and insulin [12.7% (4.4,
      21.9)]; [8.7% (0.2, 17.8)]. These differences attenuated to non-significance when
      adjusted for confounders and/or current offspring characteristics including BMI
      or body fat percentage. OGDM showed lower sex hormone binding globulin [SHBG;
      men: -12.4% (-20.2, -3.9), women: -33.2% (-46.3, -16.8)], high-density
      lipoprotein [-6.6% (-10.9, -2.2)] and apolipoprotein A1 [-4.5% (-7.5, -1.4),
      these differences survived the aforementioned adjustments. Heart rate and other
      biomarkers were similar between groups. CONCLUSIONS: Adult offspring of mothers
      with GDM have increased markers of insulin resistance and a more atherogenic
      lipid profile; these are only partly explained by confounders or current
      offspring adiposity. Maternal pre-pregnancy overweight/obesity is associated with
      impaired offspring glucose regulation, which is explained by confounders and/or
      current adiposity.
CI  - Copyright (c) 2019 Endocrine Society.
FAU - Kaseva, Nina
AU  - Kaseva N
AD  - National Institute for Health and Welfare, Helsinki and Oulu, Finland.
FAU - Vaarasmaki, Marja
AU  - Vaarasmaki M
AD  - National Institute for Health and Welfare, Helsinki and Oulu, Finland.
AD  - PEDEGO Research Unit (Research Unit for Pediatrics, Dermatology, Clinical
      Genetics, Obstetrics and Gynecology), Medical Research Center Oulu (MRC Oulu),
      Oulu University Hospital and University of Oulu, Oulu, Finland.
FAU - Sundvall, Jouko
AU  - Sundvall J
AD  - National Institute for Health and Welfare, Helsinki and Oulu, Finland.
FAU - Matinolli, Hanna-Maria
AU  - Matinolli HM
AD  - National Institute for Health and Welfare, Helsinki and Oulu, Finland.
AD  - Department of Nursing Science, University of Turku, Turku, Finland.
FAU - Sipola, Marika
AU  - Sipola M
AD  - National Institute for Health and Welfare, Helsinki and Oulu, Finland.
AD  - PEDEGO Research Unit (Research Unit for Pediatrics, Dermatology, Clinical
      Genetics, Obstetrics and Gynecology), Medical Research Center Oulu (MRC Oulu),
      Oulu University Hospital and University of Oulu, Oulu, Finland.
AD  - Institute of Health Sciences, University of Oulu, Oulu, Finland.
FAU - Tikanmaki, Marjaana
AU  - Tikanmaki M
AD  - National Institute for Health and Welfare, Helsinki and Oulu, Finland.
AD  - Institute of Health Sciences, University of Oulu, Oulu, Finland.
FAU - Heinonen, Kati
AU  - Heinonen K
AD  - Department of Psychology and Logopedics, University of Helsinki, Helsinki,
      Finland.
FAU - Lano, Aulikki
AU  - Lano A
AD  - Children's Hospital, Pediatric Research Center, Helsinki University Hospital and 
      University of Helsinki, Helsinki, Finland.
FAU - Wehkalampi, Karoliina
AU  - Wehkalampi K
AD  - Children's Hospital, Pediatric Research Center, Helsinki University Hospital and 
      University of Helsinki, Helsinki, Finland.
FAU - Wolke, Dieter
AU  - Wolke D
AD  - Department of Psychology, University of Warwick, Warwick, United Kingdom.
FAU - Ruokonen, Aimo
AU  - Ruokonen A
AD  - NordLab Oulu, Oulu University Hospital, Oulu, Finland.
AD  - Department of Clinical Chemistry, University of Oulu, Oulu, Finland.
FAU - Andersson, Sture
AU  - Andersson S
AD  - Children's Hospital, Pediatric Research Center, Helsinki University Hospital and 
      University of Helsinki, Helsinki, Finland.
FAU - Jarvelin, Marjo-Riitta
AU  - Jarvelin MR
AD  - Department of Epidemiology and Biostatistics, MRC-PHE Centre for Environment &
      Health, School of Public Health, Imperial College London, London, UK.
AD  - Center for Life Course Health Research, Faculty of Medicine, University of Oulu, 
      Oulu, Finland.
AD  - Biocenter Oulu, University of Oulu, Oulu, Finland.
AD  - Unit of Primary Care, Oulu University Hospital, Oulu, Finland.
AD  - Department of Life Sciences, College of Health and Life Sciences, Brunel
      University London, Kingston Lane, Uxbridge, Middlesex UB8 3PH, United Kingdom.
FAU - Raikkonen, Katri
AU  - Raikkonen K
AD  - Department of Psychology and Logopedics, University of Helsinki, Helsinki,
      Finland.
FAU - Eriksson, Johan G
AU  - Eriksson JG
AD  - National Institute for Health and Welfare, Helsinki and Oulu, Finland.
AD  - Department of General Practice and Primary Health Care, University of Helsinki
      and Helsinki University Hospital, Helsinki, Finland.
AD  - Folkhalsan Research Center, Helsinki, Finland.
FAU - Kajantie, Eero
AU  - Kajantie E
AD  - National Institute for Health and Welfare, Helsinki and Oulu, Finland.
AD  - PEDEGO Research Unit (Research Unit for Pediatrics, Dermatology, Clinical
      Genetics, Obstetrics and Gynecology), Medical Research Center Oulu (MRC Oulu),
      Oulu University Hospital and University of Oulu, Oulu, Finland.
AD  - Children's Hospital, Pediatric Research Center, Helsinki University Hospital and 
      University of Helsinki, Helsinki, Finland.
AD  - Department of Clinical and Molecular Medicine, Norwegian University of Science
      and Technology, Trondheim, Norway.
LA  - eng
PT  - Journal Article
DEP - 20190305
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
EDAT- 2019/03/06 06:00
MHDA- 2019/03/06 06:00
CRDT- 2019/03/06 06:00
PHST- 2018/12/19 00:00 [received]
PHST- 2019/02/25 00:00 [accepted]
PHST- 2019/03/06 06:00 [entrez]
PHST- 2019/03/06 06:00 [pubmed]
PHST- 2019/03/06 06:00 [medline]
AID - 5368422 [pii]
AID - 10.1210/jc.2018-02743 [doi]
PST - aheadofprint
SO  - J Clin Endocrinol Metab. 2019 Mar 5. pii: 5368422. doi: 10.1210/jc.2018-02743.