title: Glutamic acid decarboxylase autoantibody-positivity post-partum is associated with impaired β-cell function in women with gestational diabetes mellitus.
abstract: OBJECTIVE
  To investigate whether the presence of glutamic acid decarboxylase (GAD) autoantibodies post-partum in women with prior gestational diabetes mellitus was associated with changes in metabolic characteristics, including β-cell function and insulin sensitivity.
  
  
  METHODS
  During 1997-2010, 407 women with gestational diabetes mellitus were offered a 3-month post-partum follow-up including anthropometrics, serum lipid profile, HbA1c and GAD autoantibodies, as well as a 2-h oral glucose tolerance test (OGTT) with blood glucose, serum insulin and C-peptide at 0, 30 and 120 min. Indices of insulin sensitivity and insulin secretion were estimated to assess insulin secretion adjusted for insulin sensitivity, disposition index (DI).
  
  
  RESULTS
  Twenty-two (5.4%) women were positive for GAD autoantibodies (GAD+ve) and the remainder (94.6%) were negative for GAD autoantibodies (GAD-ve). The two groups had similar age and prevalence of diabetes mellitus. Women who were GAD+ve had significantly higher 2-h OGTT glucose concentrations during their index-pregnancy (10.5 vs. 9.8 mmol/l, P = 0.001), higher fasting glucose (5.2 vs. 5.0 mmol/l, P = 0.02) and higher 2-h glucose (7.8 vs. 7.1 mmol/l, P = 0.05) post-partum. Fasting levels of C-peptide and insulin were lower in GAD+ve women compared with GAD-ve women (520 vs. 761 pmol/l, P = 0.02 and 33 vs. 53 pmol/l, P = 0.05) Indices of insulin sensitivity were similar in GAD+ve and GAD-ve women, whereas all estimates of DI were significantly reduced in GAD+ve women.
  
  
  CONCLUSIONS
  GAD+ve women had higher glucose levels and impaired insulin secretion adjusted for insulin sensitivity (DI) compared with GAD-ve women. The combination of OGTT and GAD autoantibodies post-partum identify women with impaired β-cell function. These women should be followed with special focus on development of Type 1 diabetes.
authors.affiliation: Department of Endocrinology, Odense University Hospital, Odense, Denmark; The Clinical Research Institute, University of Southern Denmark, Odense, Denmark.
authors.forename: T P
authors.initials: TP
authors.lastname: Lundberg
authors.forename: K
authors.initials: K
authors.lastname: Højlund
authors.forename: L S
authors.initials: LS
authors.lastname: Snogdal
authors.forename: D M
authors.initials: DM
authors.lastname: Jensen
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000032:analysis*; D001327:Autoimmune Diseases / Q000175:diagnosis* / Q000453:epidemiology / Q000209:etiology / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D015331:Cohort Studies; D003718:Denmark / Q000453:epidemiology; D003922:Diabetes Mellitus, Type 1 / Q000175:diagnosis* / Q000453:epidemiology / Q000209:etiology / Q000276:immunology; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology / Q000276:immunology; D016640:Diabetes, Gestational / Q000097:blood / Q000276:immunology / Q000503:physiopathology*; D003937:Diagnosis, Differential; D042241:Early Diagnosis; D005260:Female; D005500:Follow-Up Studies; D005968:Glutamate Decarboxylase / Q000037:antagonists & inhibitors / Q000276:immunology*; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000276:immunology / Q000378:metabolism*; D049590:Postpartum Period; D011247:Pregnancy; D015995:Prevalence; D011446:Prospective Studies
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; D007328:Insulin; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2