title: The role of late-onset autoimmune diabetes in white familial NIDDM pedigrees.
abstract: OBJECTIVE
  To determine whether autoimmunity is a prominent feature of NIDDM among diabetic members in families with a strong history of NIDDM or in families with a mixture of NIDDM and IDDM.
  
  
  METHODS
  We determined GAD and islet cell (ICA512) autoantibodies from 215 NIDDM individuals and from 14 individuals with impaired glucose tolerance (IGT) of 68 families, including 1 family with maturity-onset diabetes of the young (MODY) and 3 families ascertained specifically for a mixture of NIDDM and IDDM. We tested 2 control populations: 50 unrelated spouses form Utah families, including 29 spouses with either IGT or NIDDM and 198 random nondiabetic white individuals from Colorado.
  
  
  RESULTS
  We detected either GAD or ICA512 autoantibodies in 11 members of seven families and in one spouse used as a control subject. In two families, two affected individuals showed evidence of autoimmunity, but NIDDM individuals in each of the seven families showed no evidence of autoimmunity. Among the five families with both IDDM and NIDDM individuals (three families ascertained for a mixture and two families ascertained with an incidental IDDM child), antibodies were detected in members of only one family. Antibody-positive individuals were significantly younger at diabetes onset and had low waist-to-hip ratios, but were not more likely to be insulin treated.
  
  
  CONCLUSIONS
  Autoimmunity is an important cause of apparent NIDDM, even among families with a strong history of NIDDM. However, autoimmunity among affected family members appeared to be a chance event and not the manifestation of a different genetic cause of diabetes.
authors.affiliation: Division of Endocrinology, Diabetes and Metabolism, McClellan Memorial Veterans Affairs Hospital, Little Rock, AR 72205, USA. sce@nidgenel.uams.edu
authors.forename: S C
authors.initials: SC
authors.lastname: Elbein
authors.forename: K
authors.initials: K
authors.lastname: Wegner
authors.forename: C
authors.initials: C
authors.lastname: Miles
authors.forename: L
authors.initials: L
authors.lastname: Yu
authors.forename: G
authors.initials: G
authors.lastname: Eisenbarth
mesh_terms: D000328:Adult; D017668:Age of Onset; D000368:Aged; D001323:Autoantibodies / Q000032:analysis*; D001324:Autoantigens / Q000276:immunology; D015551:Autoimmunity / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics* / Q000276:immunology*; D005260:Female; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006801:Humans; D007515:Islets of Langerhans / Q000276:immunology; D008297:Male; D008565:Membrane Proteins / Q000276:immunology*; D008875:Middle Aged; D010375:Pedigree; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases / Q000276:immunology*; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8; D044465:White People
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D008565:Membrane Proteins; C516862:PTPRN protein, human; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D017027:Protein Tyrosine Phosphatases; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8; D005968:Glutamate Decarboxylase