Possible role of hypothalamus and hypophysis in the control of development of pancreas reactivity to the effect of glucose in rat fetuses.

Abstract

To estimate the role of hypothalamus and hypophysis in the development of functional activity of pancreas, the changes of reactivity of pancreatic B-cells to glucose resulting from encephalectomy and decapitation of fetuses were investigated. Reactivity of pancreas was determined by the changes of insulin secretion induced by the addition of glucose into incubation medium. It was found that, when hypophysis and hypothalamus were removed as a result of decapitation of fetuses from normal or from diabetic pregnant rats on days 17.5-18.5 of development, their pancreas remained insensitive to glucose on 21.5 day. Removal of hypothalamus only when fetuses were encephalectomized on day 17.5 of development also resulted in the loss of sensitivity of fetal pancreas to glucose. Injection of hypothalamus homogenate to encephalectomized fetuses restored the stimulating effect of glucose on B-cells. When pancreas fragments of decapitated fetuses were preincubated together with adenohypophyses of adult rats, the decapitation effect was eliminated, and an increase of glucose concentration in the medium caused an intensive release of insulin. Similar restoring effect was induced by growth hormone (GH) and adrenocorticotrophin (ACTH) when used in in vivo and in vitro experiments. The data obtained give evidence of a possible contribution of hypothalamus and hypophysis to the control of the development of functional activity of pancreas in rat prenatal ontogenesis. However, the mechanism of this regulation remains unclear yet.