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Hormonal Regulation of the Peripubertal Surge of Insulin-Like Growth Factor-I in the Rat^*

Department of Medicine, University of Sydney and Department of Endocrinology, Royal Prince Alfred Hospital Sydney 2006, Australia

Address correspondence and requests for reprints to: Dr. David J. Handelsman, Department of Medicine, University of Sydney, Sydney 2006, New South Wales, Australia.

Abstract

The marked increase in circulating insulin-like growth factor-I (IGF-I) levels during puberty observed in primates indicates an important functional relationship between hypothalamic-pituitary gonadal function and hormonal regulation of peripubertal circulating IGF-I levels. Recent studies demonstrating local production and secretion of gonadal peptides including IGF-I suggest that increased circulating IGF-I levels during puberty might be due to direct gonadal secretion of IGF-I or alternatively to indirect effects of increased gonadal steroid secretion on nongonadal tissues including the hypothalamus, pituitary, and liver. We therefore studied the effects of prepubertal castration on the pubertal IGF-I surge and demonstrate that castration provokes a further increase rather than ablation of the pubertal IGF-I surge in the rat. Furthermore, neonatal treatment with monosodium glutamate, a hypothalamic neurotoxin, abolishes the pubertal IGF-I surge when commenced on postnatal day 1 but not on day 5, whereas treatment with a GnRH antagonist commencing within 12 h of birth significantly reduces but does not abolish the pubertal IGF-I surge. We therefore propose that the pubertal IGF-I surge in the rat is not due to direct gonadal secretion of IGF-I or other gonadal hormones during puberty but may involve hypothalamic and/or hepatic programming by events during prenatal or very early postnatal life. (Endocrinology 120: 491–496, 1987)

Footnotes

^* This work was supported by the National Health and Medical Research Council of Australia and was presented in part at the 68th Annual Meeting of The Endocrine Society, Anaheim, CA, 1986.

Received August 12, 1986.

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