INSULIN SECRETION AND IMMUNO-GENETIC MARKERS IN DIABETICS WITH SECONDARY FAILURE‘ OF ORAL HYPOGLYCEMIC AGENTS

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Abstract
Secondary failure of oral hypoglycemics, in non-insulin dependent diabetics, has been attributed to dietary non-compliance, inadequate drug dosage, metabolic stress or true drug failure. Progressive loss of .beta. cell function is a suggested mechanism for true drug failure but on the basis of little documented evidence. Basal and glucagon-stimulated C-peptide levels, HLA types and islet cell antibodies in 20 non-insulin dependent diabetics with secondary failure of oral agents were measured. There were 16 females and 4 males with a mean ideal body weight of 1.30 units and mean duration of diabetes of 9.5 yr. Fasting insulin (mean .+-. SD; 15.1 .+-. 10.6 mU/l) and fasting C-peptide (2.3 .+-. 1.2 .mu.g/l) were normal or slightly elevated in all but 1 patient. Mean C-peptide increased from 2.3 .+-. 1.2 .mu.g/l to 3.5 .+-. 2.2 .mu.g/l (152% over basal) 6 min after 1 mg i.v. glucagon. In 15 patients the C-peptide response was greater than 130% of basal. Islet cell cytoplasmic antibodies were detected in only 2 patients. The distribution of HLA types was not significantly different from a control population, with no increase in DR3 or DR4. Thus, absolute insulin deficiency is uncommon in non-insulin dependent diabetics with secondary failure of oral hypoglycemic agents and such patients do not exhibit the immuno-genetic markers of insulin-dependent diabetes.