Insulin-Like Growth Factor Binding Protein-1 Induces Insulin Release in the Rat

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Abstract
Injections of human insulin-like growth factor binding protein (hIGFBP-1) are reported to induce hyperglycemia in the rat, sug- gesting that IGFBP-1 acutely regulates glucose homeostasis. We now report the effects on glucose and insulin levels of administering re- combinant (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 mg/rat). rhIGFBP-1 did not affect blood glu- cose acutely but did stimulate insulin release in normal rats (5 min post injection; PBS, 103.5 6 8.5; rhIGFBP-1 (500 mg), 166.8 6 15.7; rhIGFBP-1 (100 mg); 151.4 6 14.1% initial). rhIGFBP-1 pretreat- ment, in normal and diabetic rats, reduced the hypoglycemic response to rhIGF-I (diabetic rats after 20 min: PBS, 103.4 6 11.4; BP-1 (500 mg) 1 rhIGF-I (50 mg), 97.6 6 3.6; rhIGF-I, 48.2 6 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 sup- presses insulin secretion and imply that aberrant IGFBP levels or reduced IGF-I bioactivity may lead to chronic hyperinsulinemia. (Endocrinology 138: 2073-2080, 1997)

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