title: Declining beta-cell compensation for insulin resistance in Hispanic women with recent gestational diabetes mellitus: association with changes in weight, adiponectin, and C-reactive protein.
abstract: OBJECTIVE
  To identify factors associated with declining beta-cell compensation for insulin resistance.
  
  
  METHODS
  In a cohort of Hispanic women with recent gestational diabetes mellitus, oral glucose tolerance tests (OGTTs), intravenous glucose tolerance tests (IVGTTs), and bioelectrical impedance measurements were performed at 15-month intervals for up to 5 years, or until fasting plasma glucose exceeded 140 mg/dl (7.8 mmol/l). Data were analyzed to identify predictors of declining beta-cell compensation for insulin resistance (the disposition index [DI]) and to examine the mechanism of weight gain and changes in circulating levels of selected adipokines and inflammatory markers on beta-cell compensation decline.
  
  
  RESULTS
  A total of 60 nondiabetic women had a median of four sets of OGTT + IVGTT during a median follow-up of 52 months. Fourteen of the women developed diabetes. None of the baseline characteristics were significantly predictive of a decline in DI. There were significant univariate associations between declining DI and weight gain (specifically fat gain), declining adiponectin and rising C-reactive protein. Multivariate analysis showed that the weight gain was the most significant factor associated with declining DI. The amount of association between weight gain and declining DI was explained 31% by changes in adiponectin and C-reactive protein and 40% by changes in insulin resistance.
  
  
  CONCLUSIONS
  These results identify weight gain as the strongest factor associated with declining beta-cell compensation for insulin resistance in Hispanic women at high risk for type 2 diabetes. Such effect may be mediated through at least two effects: alterations in adipokine levels and increasing insulin resistance.
authors.affiliation: Department of Preventive Medicine, University of Southern California School of Medicine, Los Angeles, California, USA. xiang@usc.edu
authors.forename: Anny H
authors.initials: AH
authors.lastname: Xiang
authors.forename: Miwa
authors.initials: M
authors.lastname: Kawakubo
authors.forename: Enrique
authors.initials: E
authors.lastname: Trigo
authors.forename: Siri L
authors.initials: SL
authors.lastname: Kjos
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Buchanan
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000273:Adipose Tissue / Q000033:anatomy & histology; D000328:Adult; D001835:Body Weight; D002097:C-Reactive Protein / Q000378:metabolism*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D016640:Diabetes, Gestational / Q000097:blood / Q000503:physiopathology*; D017097:Electric Impedance; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000502:physiology*; D020738:Leptin / Q000097:blood; D011247:Pregnancy; D014280:Triglycerides / Q000097:blood
chemical_list: D052242:Adiponectin; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D020738:Leptin; D014280:Triglycerides; D002097:C-Reactive Protein