title: Diabetes autoantibodies do not predict progression to diabetes in adults: the Diabetes Prevention Program.
abstract: To determine if the presence of diabetes autoantibodies predicts the development of diabetes among participants in the Diabetes Prevention Program.
  
  
  
  A total of 3050 participants were randomized into three treatment groups: intensive lifestyle intervention, metformin and placebo. Glutamic acid decarboxylase (GAD) 65 autoantibodies and insulinoma-associated-2 autoantibodies were measured at baseline and participants were followed for 3.2 years for the development of diabetes.
  
  
  
  The overall prevalence of GAD autoantibodies was 4.0%, and it varied across racial/ethnic groups from 2.4% among Asian-Pacific Islanders to 7.0% among non-Hispanic black people. There were no significant differences in BMI or metabolic variables (glucose, insulin, HbA(1c), estimated insulin resistance, corrected insulin response) stratified by baseline GAD antibody status. GAD autoantibody positivity did not predict diabetes overall (adjusted hazard ratio 0.98; 95% CI 0.56-1.73) or in any of the three treatment groups. Insulinoma-associated-2 autoantibodies were positive in only one participant (0.033%).
  
  
  
  These data suggest that 'diabetes autoimmunity', as reflected by GAD antibodies and insulinoma-associated-2 autoantibodies, in middle-aged individuals at risk for diabetes is not a clinically relevant risk factor for progression to diabetes.
authors.affiliation: Department of Epidemiology, University of Colorado at Denver, Colorado School of Public Health, Aurora, CO, USA.
authors.forename: D
authors.initials: D
authors.lastname: Dabelea
authors.forename: Y
authors.initials: Y
authors.lastname: Ma
authors.forename: W C
authors.initials: WC
authors.lastname: Knowler
authors.forename: S
authors.initials: S
authors.lastname: Marcovina
authors.forename: C D
authors.initials: CD
authors.lastname: Saudek
authors.forename: R
authors.initials: R
authors.lastname: Arakaki
authors.forename: N H
authors.initials: NH
authors.lastname: White
authors.forename: S E
authors.initials: SE
authors.lastname: Kahn
authors.forename: T J
authors.initials: TJ
authors.lastname: Orchard
authors.forename: R
authors.initials: R
authors.lastname: Goldberg
authors.forename: J
authors.initials: J
authors.lastname: Palmer
authors.forename: R F
authors.initials: RF
authors.lastname: Hamman
mesh_terms: D001323:Autoantibodies / Q000097:blood* / Q000276:immunology; D015551:Autoimmunity; D001786:Blood Glucose / Q000378:metabolism; D003920:Diabetes Mellitus / Q000276:immunology* / Q000517:prevention & control; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000276:immunology / Q000378:metabolism; D007333:Insulin Resistance / Q000276:immunology; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000378:metabolism*; D008297:Male; D008687:Metformin / Q000627:therapeutic use*; D008875:Middle Aged; D011237:Predictive Value of Tests; D015995:Prevalence; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8 / Q000276:immunology*; D040242:Risk Reduction Behavior; D016896:Treatment Outcome
chemical_list: D001323:Autoantibodies; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D008687:Metformin; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8; D005968:Glutamate Decarboxylase