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Insulin-like growth factor I: a possible metabolic signal involved in the regulation of female puberty.

In both rats and primates, including humans, serum levels of insulin-like growth factor I (IGF-I) increase during the onset of puberty, suggesting a role for IGF-I in this process. We examined the ability of IGF-I to affect the release of hypothalamic luteinizing hormone releasing hormone (LHRH) in prepubertal female rats. Our results indicate that IGF-I acts on the median eminence, which contains the highest density of type 1 IGF receptors in the brain, to elicit a dose-related increase in LHRH release. In this regard, a minimal effective dose of 10 ng/ml (p less than 0.05) and a maximal effective dose of 100 ng/ml (p less than 0.01) was observed. IGF-II and insulin were one order of magnitude less effective. The results demonstrate that IGF-I has the capability to act directly upon the median eminence to effect release of LHRH, thereby suggesting a role for IGF-I in facilitating peripubertal changes in LHRH release. Thus, IGF-I may represent one of the 'metabolic signals' thought to be involved in the initiation of puberty.