The hypoglycaemic action of somatostatin was investigated in fasted anaesthetized dogs. An isotopic turnover technique with radioactive D-[2-3H] glucose tracer was used to measure the rates of hepatic production and peripheral utilization of glucose before, during, and after a 60min infusion of 150 mug somatostatin. Plasma concentrations of insulin, glucagon, growth hormone, cortisol and free fatty acids were also measured. Somatostatin infusion caused a fall of plasma glucose demonstrable within 10 min. After 60 min plasma glucose had fallen to 75% of the pre-infusion concentration. Simultaneoulsy the specific activity of the D-[2-3H] glucose increased and calculation of the rates of production and utilization of glucose over 10 min intervals indicated that the mean hepatic production rate of glucose fell to 59% of the pre-infusion rate while the rate of peripheral utilization of glucose fell to 83% of the pre-infusion rate. These results show that the hypoglycaemic action of intravenous somatostatin depends exclusively upon the inhibition of hepatic glucose production. This effect may have been partly due to a fall of plasma glucagon concentration and occurred despite a fall of plasma insulin to less than 1 mu 1(-1).
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Blauth et al. (1977) studied this question.
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