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Departments of Endocrinology and Process Sciences, Genentech, Inc., South San Francisco, California 94080
Address all correspondence and requests for reprints to: Dr. R. G. Clark, Mail Stop 37, Department of Endocrinology, Genentech, Inc., 390 Point San Bruno Boulevard, South San Francisco, California 94080. E-mail: rossc{at}gene.com
Injections of human insulin-like growth factor binding protein (hIGFBP-1) are reported to induce hyperglycemia in the rat, suggesting that IGFBP-1 acutely regulates glucose homeostasis. We now report the effects on glucose and insulin levels of administering recombinant (r) hIGFBP-1.
In a series of studies, normal and streptozotocin (STZ) diabetic male Wistar rats (180–210 g), fasted for 6 or 16 h, were injected with rhIGFBP-1 (iv, 80–500 µg/rat). rhIGFBP-1 did not affect blood glucose acutely but did stimulate insulin release in normal rats (5 min post injection; PBS, 103.5 ± 8.5; rhIGFBP-1 (500 µg), 166.8 ± 15.7; rhIGFBP-1 (100 µg); 151.4 ± 14.1% initial). rhIGFBP-1 pretreatment, in normal and diabetic rats, reduced the hypoglycemic response to rhIGF-I (diabetic rats after 20 min: PBS, 103.4 ± 11.4; BP-1 (500 µg) + rhIGF-I (50 µg), 97.6 ± 3.6; rhIGF-I, 48.2 ± 4.3% initial) but did not affect the hypoglycemic response to des(1–3)IGF-I or insulin (0.5 U/kg).
These studies show that rhIGFBP-1 causes insulin release, has a minimal effect on blood glucose, and inhibits the hypoglycemic effect of rhIGF-I. These data suggest that endogenous IGF-I tonically suppresses insulin secretion and imply that aberrant IGFBP levels or reduced IGF-I bioactivity may lead to chronic hyperinsulinemia.
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