Serum IGF-1 and Binding Proteins 1 and 3 in Postmenopausal Women and the Effects of Estrogen

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Abstract
Few data exist on the insulin-like growth factor (IGF) axis in postmenopausal women, particularly on the effects of estrogen on the IGF binding proteins (BPs). Although serum IGF-BP1 (BPI) levels are regulated primarily by pancreatic hormones (insulin and somatostatin), a role For estrogens has been suggested. We studied 14 postmenopausal women [mean age. 54.8 ± 0.6 years: (BMI) body mass index 23.8 ± 1] before and after oral estrogen (2 mg/day of micronized estradiol for 3 months). Ten normal premenopausal women (mean age. 28.7 ± I years: mean BMI, 23.1 ± 1) served as controls. Serum IGF-I. IGF-BP3 (BP3), BPI, and insulin were measured before and after estrogen. The ratio of IGF-I/BP3 was calculated, as was the ratio of IGF-1/BPI. Glucose and BPI sensitivity to insulin was measured after insulin administration (0.1 U/kg. with blood samples obtained at 0. 2. 5. 10. 15. and 30 min). Before treatment, postmenopausal women had fasting insulin levels (60 ± 3 pM), IGF-1 (32 ± 3 nM). BP3 (155 ± 10 nM); and BPI (0.12 ± 0.02 nM) that were similar to the values in premenopausal women. Insulin administration revealed a reduced glucose disappearance (reduced insulin sensitivity) and a blunted BPI decrease in postmenopausal women compared to normal women (p < 0.05). After 3 months of estrogen, serum IGF-I levels decreased (22.3 ± n.M.p < 0.05) and serum BPI increased (0.24 ± 0.03 nM:p < 0.05). while BP3 and insulin levels were unchanged. The ratio of IGFI/BP3 was not significantly reduced but the ratio of IGF-1/BPI decreased (p < 0.05). Insulin and BPI sensitivity was improved after estrogen, although not significantly. In conclusion, oral estrogen increases BPI in postmenopausal women, probably by stimulating its hepatic secretion and without modifying insulin levels. Because BPI reduces the biologic activity of IG F-I on several tissues including the ovary, estrogens may decrease IGF-1 stimulated ovarian androgen secretion. Some metabolic effects of estrogens may be mediated by changes in the biologic activity of IGF-1.