Abstract

The hypothesis that the timing of puberty is at least in part stimulated by some 'metabolic signal' that tells the central control system of the reproductive axis that the body is becoming large enough, and that there are enough metabolic fuel stores, to support reproductive function has received considerable attention over the past several decades. However, direct experimental support for the hypothesis that mild metabolic changes, such as those that occur slowly during development, are actually capable of modulating reproductive function has been lacking. Our recent studies have shown that very brief periods of fasting in both male rhesus monkeys and men can modify the pulsatile release of LH and testosterone. In monkeys, missing a single meal is associated with a suppression of mean plasma LH, FSH and testosterone concentrations, and with a slowing of the frequency of pulsatile LH secretion. Current studies are aimed at identifying the specific metabolic signals which cause these changes. It is hoped that the results of these studies will eventually help to answer the question of whether normal metabolic changes occurring during development play a role in timing puberty onset.

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