The Diabetogenic Action of Somatostatin in Healthy Subjects and in Maturity Onset Diabetics*

Abstract

To determine whether cyclic somatostatin (GH-RIH) interferes with glucose utilization and gluconeogenesis we studied levels of blood glucose (BG), immunoreactive insulin (IRI), immunoreactive glucagon (IRG) and of human growth hormone (GH) after iv glucose (330 mg/kg) and iv arginine (0,5 g/kg) in healthy subjects (n= 8) and in maturity onset diabetics (n= 8/ fasting BG11 = 0.55±0.14 (SE)%per min; kn= 0.42±0.03 (SE)%per min). The response of insulin to glucose was abolished by GH-RIH. The glucose induced suppression of IRG was in part significantly enhanced by GH-RIH in maturity onset diabetics (P<0.01). BG rises seen after iv arginine were increased by the administration of GH-RIH both in healthy subjects (P<0.001) and in maturity onset diabetics (P<0.05). Somatostatin abolished IRI and GH responses to arginine in both groups studied (P<0.001). IRG increases after arginine administration were diminished by GH-RIH in both groups (P<0.01). Our data demonstrate that GH-RIH impairs the iv carbohydrate tolerance in healthy subjects and facilitates an increased hepatic glucose output upon administration of arginine both in controls and in maturity onset diabetics. We attribute the diabetogenic effect of somatostatin to suppression of IRI release rather than to changes in the IRG/IRI ratio in favor of IRG.