Hyperinsulinämie und B‐Zellproliferation in postnatal mit L‐Glutamat behandelten Ratten

Abstract

Development of hyperinsulinemia was investigated which appeared late in the obese state in rats postnatally treated with L-glutamate. Insulin concentrations were estimated in the blood plasma of the caval and portal vein, and morphometric and immunohistochemical measurements of cells in the islets of Langerhans were performed, and also glucose tolerance tests. Not earlier than at 3 months hyperinsulinemia is shown in glutamate obese rats (GOR) in the peripheral blood plasma. Also in the portal blood plasma the insulin concentration is higher (167%) in GOR relative to controls. The insulin concentrations in the portal vein rise further in both animal groups whereas insulin concentration in the peripheral blood remains at the different levels in both animal groups. Impaired glucose tolerance was observed for GOR only. Islets of Langerhans in the Pancreas show enlargement and increased proliferation of B-cells in GOR. In contrast the number of D-cells is diminished. The hyperplasia of islets differs remarkably to hypoplasia of other organs in GOR. We conclude that the peripheral hyperinsulinemia is caused by a permanent hypersecretion of insulin.

In vivo Assessment of Insulin Binding in Different Organs of Growing and Adult Glutamate-Induced Obese Rats

“…In contrast to other animal models of obesity, accumulation of triglycerides is not accompanied by peripheral hyperinsulinemia (Pöge et al, 1990).…”

“…From these findings it may be concluded that hyperinsulinemia of glutamate-induced obese rats can not be attributed to diminished organ specific insulin binding. More likely an age dependent increase in insulin secretion of n-cells of pancreas (Pöge et al, 1990) may cause the development of peripheral hyperinsulinemia. Despite of hyperinsulinemia and unchanged insulin binding of obese rats altered insulin sensitivity is possible may be as a result of postreceptor defects.…”