Metabolic Cues for the Onset of Puberty

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.

Reproductive ecology and life history of the human male

“…Ellison (1997) proposed that environmental conditions affecting energy availability during human female puberty may underlie variation in adult ovarian function. While the role of hormonal priming in male adolescents remains to be fully elucidated, variation in HPT function and pubertal development in association with energy availability has been documented in rodents, nonhuman primates, and humans (Cameron, 1991;Dubey et al, 1986;Jean-Faucher et al, 1982;Kulin, 1996;Kulin et al, 1982Kulin et al, , 1984. Kulin et al (1984) reported that undernourished Kenyan male adolescents exhibited delayed pubertal LH and FSH increases compared to well-fed controls living in affluent neighborhoods of Nairobi.…”

“…The site of suppression appeared to be the hypothalamus, since bolus injections of GnRH resulted in higher LH and testosterone responses in glucose-supplemented individuals compared to fasting men (Röjdmark, 1987a,b). Forty-eight-hour fasts have also been reported to alter testosterone produc-tion by decreasing LH pulse frequency (Cameron et al, 1991) as well as decreasing LH pulse amplitudes (Veldhuis et al, 1993).…”

The involvement of gonadotropin inhibitory hormone and kisspeptin in the metabolic regulation of reproduction

“…Reproduction in nonprimate mammals and in primates is highly responsive to metabolic alterations (Cameron 1991, Wade & Jones 2004. Deficiencies of metabolic fuels prevent the proper release of gonadotropin releasing hormone (GnRH) from the hypothalamus, thus causing reproductive quiescence (Bergendahl et al 1991, Wahab et al 2013a.…”

“…Deficiencies of metabolic fuels prevent the proper release of gonadotropin releasing hormone (GnRH) from the hypothalamus, thus causing reproductive quiescence (Bergendahl et al 1991, Wahab et al 2013a. Initiation of reproductive function is delayed by conditions of negative energy balance while, in adults, merely skipping one daily meal can lead to reproductive quiescence in nonhuman primates (Kennedy & Mitra 1963a, Foster & Olster 1985, Cameron 1991, 1996. Food resumption regularizes the dysfunctional reproductive axis and normalizes reproduction (Parfitt et al 1991).…”

Effect of feed restriction on serum somatotropin, insulin-like growth factor-I-(IGF-I) and IGF binding proteins in cyclic heifers actively immunized against growth hormone releasing factor

“…Kinder and coworkers (12) have suggested that feed restriction alters ovarian function through a decrease in pulsatile release of UI. Metabolic signal( s) through which chronic feed restriction alters LH and ovarian function have not been elucidated (15,16,17,18).…”