Immunocytochemical localization of prolactin-like immunoreactivity in rat pancreatic islets

Animal experiments and clinical data indicate that prolactin (PRL) induces hyperinsulinemia and even diabetes. The effects of PRL on carbohydrate metabolism may be explained by at least two different mechanisms. Either PRL induces an insulin resistance at the peripheral tissue level, or PRL has a direct cytotropic effect on the pancreatic islets. Obviously, both mechanisms inducing hyperinsulinemia may coexist. We report here immunocytochemical evidence that PRL is localized in the endocrine pancreas of the normal adult rat. More precisely, the immunoreactive PRL is distributed in the cytoplasm of insulin-secreting B cells. These findings support a direct action of PRL on the endocrine pancreas.