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At birth newborn rats from mothers with experimentally induced diabetes show hypertrophy and degranulation of the pancreatic islets. With birth the maternal hyperglycaemic stimulus is removed and during the lactation period the overstimulated B cells can restore their normal secretory activity. The increase of B-cell mass, however, remains retarded for several weeks. By adulthood the endocrine pancreas of offspring from mildly diabetic mothers seems to have recovered from the influence of the abnormal intra-uterine milieu, at least as judged by morphometric examination. In offspring from severely diabetic mothers an increased secretory activity of the individual B cells might be responsible for their sustained hypoglycaemia.