PMID- 25231898
OWN - NLM
STAT- MEDLINE
DCOM- 20150616
LR  - 20220321
IS  - 1935-5548 (Electronic)
IS  - 0149-5992 (Linking)
VI  - 37
IP  - 12
DP  - 2014 Dec
TI  - Each degree of glucose intolerance in pregnancy predicts distinct trajectories of 
      beta-cell function, insulin sensitivity, and glycemia in the first 3 years 
      postpartum.
PG  - 3262-9
LID - 10.2337/dc14-1529 [doi]
AB  - OBJECTIVE: Glucose intolerance in pregnancy predicts an increased risk of future 
      type 2 diabetes mellitus (T2DM) that is proportional to the severity of 
      antepartum dysglycemia (i.e., highest in women with gestational diabetes mellitus 
      [GDM], followed by those with milder dysglycemia). However, the pathophysiologic 
      changes driving this risk are not known. Thus, we evaluated the longitudinal 
      changes in beta-cell function, insulin sensitivity, and glycemia in the first 3 
      years postpartum after gestational dysglycemia. RESEARCH DESIGN AND METHODS: A 
      total of 337 women underwent glucose challenge test (GCT) and oral glucose 
      tolerance test (OGTT) in pregnancy, followed by repeat OGTT at 3 months, 1 year, 
      and 3 years postpartum. The antepartum GCT/OGTT identified four gestational 
      glucose tolerance groups: GDM (n = 105); gestational impaired glucose tolerance 
      (GIGT; n = 60); abnormal GCT, followed by normal glucose tolerance (NGT) on the 
      OGTT (abnormal GCT NGT; n = 96); and normal GCT with NGT (n = 76). RESULTS: At 
      each of 3 months, 1 year, and 3 years postpartum, the prevalence of glucose 
      intolerance increased from normal GCT NGT to abnormal GCT NGT to GIGT to GDM (all 
      P < 0.001), whereas beta-cell function, assessed by the Insulin 
      Secretion-Sensitivity Index-2 (ISSI-2), and insulin sensitivity (Matsuda index), 
      progressively decreased across the groups (all P < 0.002). Each group predicted 
      distinct trajectories of ISSI-2, Matsuda index, and fasting and 2-h glucose (all 
      P < 0.001). Notably, GDM, GIGT, and abnormal GCT NGT predicted varying rates of 
      declining beta-cell function and insulin sensitivity, as well as rising glycemia, 
      compared with normal GCT NGT. CONCLUSIONS: Each degree of gestational glucose 
      intolerance predicts distinct trajectories of beta-cell function, insulin 
      sensitivity, and glycemia in the first 3 years postpartum that drive their 
      differential risk of future T2DM.
CI  - (c) 2014 by the American Diabetes Association. Readers may use this article as long 
      as the work is properly cited, the use is educational and not for profit, and the 
      work is not altered.
FAU - Kramer, Caroline K
AU  - Kramer CK
AD  - Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, 
      Canada Division of Endocrinology, University of Toronto, Toronto, Ontario, 
      Canada.
FAU - Swaminathan, Balakumar
AU  - Swaminathan B
AD  - Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, 
      Canada.
FAU - Hanley, Anthony J
AU  - Hanley AJ
AD  - Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, 
      Canada Division of Endocrinology, University of Toronto, Toronto, Ontario, Canada 
      Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, 
      Canada.
FAU - Connelly, Philip W
AU  - Connelly PW
AD  - Division of Endocrinology, University of Toronto, Toronto, Ontario, Canada Keenan 
      Research Centre for Biomedical Science of St. Michael's Hospital, Toronto, 
      Ontario, Canada Department of Laboratory Medicine and Pathobiology, University of 
      Toronto, Toronto, Ontario, Canada.
FAU - Sermer, Mathew
AU  - Sermer M
AD  - Division of Obstetrics and Gynecology, University of Toronto, Toronto, Ontario, 
      Canada.
FAU - Zinman, Bernard
AU  - Zinman B
AD  - Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, 
      Canada Division of Endocrinology, University of Toronto, Toronto, Ontario, Canada 
      Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, 
      Canada.
FAU - Retnakaran, Ravi
AU  - Retnakaran R
AD  - Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, 
      Canada Division of Endocrinology, University of Toronto, Toronto, Ontario, Canada 
      Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, 
      Canada rretnakaran@mtsinai.on.ca.
LA  - eng
GR  - 84206/Canadian Institutes of Health Research/Canada
GR  - MOP-67063/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140917
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (Blood Glucose)
SB  - IM
MH  - Adult
MH  - Blood Glucose/*metabolism
MH  - Diabetes Mellitus, Type 2/blood/*diagnosis/epidemiology/physiopathology
MH  - Diabetes, Gestational/diagnosis/epidemiology/*metabolism/*physiopathology
MH  - Disease Progression
MH  - Female
MH  - Follow-Up Studies
MH  - *Glucose Intolerance/classification/diagnosis/epidemiology
MH  - Glucose Tolerance Test
MH  - Humans
MH  - *Insulin Resistance
MH  - Insulin-Secreting Cells/*physiology
MH  - *Postpartum Period/blood/physiology
MH  - Pregnancy
MH  - Prognosis
EDAT- 2014/09/19 06:00
MHDA- 2015/06/17 06:00
CRDT- 2014/09/19 06:00
PHST- 2014/09/19 06:00 [entrez]
PHST- 2014/09/19 06:00 [pubmed]
PHST- 2015/06/17 06:00 [medline]
AID - dc14-1529 [pii]
AID - 10.2337/dc14-1529 [doi]
PST - ppublish
SO  - Diabetes Care. 2014 Dec;37(12):3262-9. doi: 10.2337/dc14-1529. Epub 2014 Sep 17.