The offspring of mother animals with mild gestational hyperglycaemia exhibited basal hyperinsulinism, decreased glucose tolerance and increased susceptibility to streptozotocin diabetes. Following low-dose successive streptozotocin treatment a significantly increased spleen cell cytotoxicity against beta-cells was found in these animals as compared to the offspring of gestational normoglycaemic control mothers. Such increased cell-mediated cytotoxicity, considered as enhanced autoimmune reactivity, was positively correlated to blood glucose levels and negatively correlated to pancreatic insulin contents. Thus, hyperinsulinism, occurring during pre- and neonatal brain organization and produced by gestational hyperglycaemia, is a predisposing teratogenetic risk factor not only for the development of type II, but also of type I diabetes. Thus, it is comprehensible that the prevalence of type I diabetes in children could be decisively reduced by preventing gestational hyperglycaemia in their mothers (Dörner et al., 1985).