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Department of Medicine, University of Toronto, Toronto, Ontario Canada
Address all correspondence and requests for reprints to: Dr. B. Zinman, 11 EN-229, Toronto General Hospital, 200 Elizabeth Street, Toronto, Ontario, M5G 2C4 Canada.
GH has been implicated in the pathophysiology of various acute and chronic complications of diabetes mellitus. As a consequence, there has been a great deal of interest in developing methods for suppressing GH secretion in diabetes. SMS 201–995 is a long-acting somatostatin analog which inhibits the secretion of numerous hormones, including GH. To determine the metabolic and hormonal responses to SMS 201–995 independent of endogenous insulin suppression, we studied six patients with insulin-dependent diabetes mellitus while they received 150 µg SMS 201–995, sc, daily for an 8-week period. This treatment resulted in no change in 24-h glucose profiles, although the mean insulin dose decreased by 19%, while hemoglobin A1c decreased significantly (0.084 ± 0.023 to 0.067 ± 0.011, P = 0.04). The 24-h profiles of blood lactate, plasma free insulin, glucagon, FFA, blood glycerol, and β-hydroxybutyrate were unchanged, whereas that ofblood alanine increased significantly (7.8 ± 0.4 to 10.6 ± 0.9 mmol/L·h; P = 0.01). GH secretion declined in five of the six patients; the meanvaluesbefore and during SMS 201–995 treatment were 102 ± 23 and 68 ± 12 µg/ L·h, respectively (P = NS), for the six patients. [In the five patients in whom GH secretion declined, the mean values before and during SMS 201–995 treatment were 115 ± 23 and 63 ± 14 µg/L·h, respectively (P = 0.01).] These results suggest that SMS 201–995 may be administered to patients with insulin-dependent diabetes mellitus without a deleterious effect on metabolic control.
Received March 30, 1988.
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