Somatostatin does not increase insulin-stimulated glucose uptake in humans

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Abstract
Somatostatin (SRIF) has been widely used in the study of in vivo carbohydrate metabolism to suppress pancreatic hormone secretion and thereby interrupt the glucoregulatory feedback loops between insulin, glucagon, and glucose. A critical assumption in the use of SRIF is that it has no effect on hepatic or peripheral glucose metabolism other than those mediated through the inhibition of hormone secretion. To assess whether doses of SRIF commonly used in human investigation have any effect on insulin-stimulated glucose disposal rates, we measured 5 ± the rate in 6 normal subjects (mean fasting serum glucose level, 93 ± 2 mg/dl) during euglycemic (≃85 mg/dl) hyperinsulinemic (40 mU · m−2 · min1) clamp studies both with and without the concomitant infusion of SRIF (600 μg/hr). The steady-state insulin levels achieved were 85 ± 6 μU/ml and 74 ± 8 (μU/ml with and without SRIF, respectively (difference not significant). Glucose disposal rates between 120 and 180 min of the clamp were 7.11 ± 0.10 and 7.35 ± 0.10 mg · kg1 · min1 with and without SRIF, respectively (difference not significant). We concluded that in doses commonly used in human investigation, SRIF does not increase glucose disposal.