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Journal of Clinical Endocrinology & Metabolism Vol. 44, No. 5 876-883
doi:10.1210/jcem-44-5-876
Copyright © 1977 by the Endocrine Society.
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The Diabetogenic Action of Somatostatin in Healthy Subjects and in Maturity Onset Diabetics*

W. WALDHÄUSL, P. BRATUSCH-MARRAIN, R. DUDCZAK and E. DEUTSCH

Medizinische Universitätsklinik (Chief: Prof. Dr. E. Deutsch), Division of Clinical Endocrinology and Diabetes Mellitus Wien, Austria.

Requests for reprints to: Werner Waldhausl, M.D., 1. Medizinische Universitatsklinik, Division of Clinical Endocrinology and Diabetes mellitus, A 1090 Wien, Austria.

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 BG<200 mg/dl) both in the presence and in the absence of GH-RIH (500 µig/h iv). GH-RIH caused a reduction of glucose utilization in healthy subjects as shown by the decrease of the k-value from 2.08±0.22 (SE)%per min to 0.61±0.06 (SE)%per min (P< 0.0005). No significant change of the glucose disappearance rate was observed in maturity onset diabetics by GH-RIH (k11 = 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.

* This work was presented in part at the 5th International Congress of Endocrinology. Hamburg, FRG, July, 1976.

Supported by grants of the "Fonds zur Forderung der wissenschaftlichen Forschung Osterreichs" Nos. M2-2777 and 3401.

Received September 8, 1976.







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