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The clinical onset of insulin-dependent diabetes (IDD) is characterized by the onset of circulation of autoantibodies to beta-cells. Thirty-three newly detected IDD patients and 14 newly detected patients with noninsulin-dependent diabetes mellitus were examined for autoantibodies to antigen P 64-69, to surface antigen of islet cells, to thyrocyte microsomal fraction, thyroglobulin, hypophysis, fibroblasts; the levels of circulating immune complexes were measured as well. IDD debut was found associated with the appearance of antibodies to pancreatic islet cells, thyroid, thyroglobulin, hypophysis, fibroblasts, this indicating a polyclonal activation of the immunity system. A relationship was revealed between antifibroblast antibody and anti-islet-cell antibody. Antihypophyseal antibodies were detected in 43% of patients with noninsulin dependent diabetes. Nine per cent of IDD patients and 24% of patients with noninsulin dependent condition were negative in the tests.

The time course of metabolic parameters and islet cell surface antibodies (ICSA) in low-dose streptozotocin (STZ)-induced diabetes in rats was studied, a total STZ dose being 160 mg/kg body weight. Two-phase diabetes development was observed. Initial mild hypoinsulinemia and hyperglycemia turned to more severe diabetes after day 24 which was preceded by the first ICSA peak at day 13. The second ICSA peak occurred at day 35. The data obtained suggest that in this model of diabetes the toxic STZ effect induces both the diabetic syndrome and humoral autoimmunity to beta-cells, and the latter leads to further impairment of diabetes.

It has been shown that before insulin treatment children with diabetes mellitus diagnosed for the first time manifested heterogenous endogenous secretion of insulin, which did not correlate with the disease standing before diagnosis establishment.