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Differential Alterations of the Circulating Prosomatostatin-Derived Peptides During Insulin-Induced Hypoglycemia in Man^*

Department of Medicine, University of Washington Seattle, Washington 98195

Address requests for reprints to: Dr. Bruce H. Francis, Department of Medicine, RC-14, University of Washington, Seattle, Washington 98195.

Insulin-induced hypoglycemia stimulates a rise of somatostatin-like immunoreactivity (SLI) in the venous circulation of man. Plasma SLI is comprised of a heterogenous group of peptides including somatostatin-28 (SS-28) somatostatin-28-(15-28), somatostatin-28-(16-28), and prosomatostatin (Pro-SS). To determine which of these Pro-SS related peptides is released after hypoglycemia, we developed an immunoadsorption method that rapidly and accurately separates SS-28 from the other somatostatins. This method involves the selective retention of SS-28 on a conjugate of agarose with immunoglobulins that recognize an epitope in the NH2-terminal region of SS-28. Pro-SS, SS-28-(15-28), SS-28-(16-28), henceforth referred to collectively as SS-28-(15-28), and SS-28, once separated, were then analyzed by RIA with a COOH-terminal antibody. Ten normal men were studied after an overnight fast. Pork insulin (0.05 U/kg) was injected iv, and blood was collected before and after the onset of hypoglycemia. The mean basal SS-28-(15-28) level was 13 ± 1 (±SEM) pg/mL, and the mean basal SS-28 levels were 19 ± 3 (±SEM) pg/mL. Plasma SS-28-(15-28) did not increase after insulin administration, but the mean SS-28 level increased by 76% (P < 0.01). We propose that the release of SS-28, presumably from the gastrointestinal tract, during hypoglycemia occurs as a result of activation of the autonomic nervous system and speculate that SS-28, because of its ability to inhibit insulin secretion, may be important in counterregulation during glucopenia.

^* Presented in part at VI International Symposium on Gastrointestinal Hormones, Vancouver, British Columbia, Canada, July 6–10, 1986. This work was supported by USPHS Grant 5-RO1-AM-34397, the V.A., NIH Grant AM-36116, Program Project Grant AM-02456, Grant AM-17047, the Diabetes Endocrinology and Research Center, the American Diabetes Association, Juvenile Diabetes Foundation, and the Sugar Association, Inc. A portion of this work was conducted through the Clinical Research Center facility of the University of Washington supported by the NIH Grant RR-37.

Received December 29, 1986.