Basic counterpoint: mechanisms and pathways of gonadal steroid modulation of growth hormone secretion.

Abstract

In spite of the different patterns of GH secretion observed in male and female rats, it can be argued that there are limited differences between the mechanism of action of androgens and estrogens as reported in the literature. However, we feel that it is possible to organize the available data into a unique physiological model explaining the sex-based differences in GH secretion in the rat. Thus, it can be proposed that the greater spontaneous GH peaks observed in the male with respect to the female rat may be due to an androgen-mediated enhancement of both GHRH secretion at the hypothalamic level and GH secretion at the pituitary level. The lower GH troughs observed in the male as compared to the female rat may be due to increased interpeak somatostatin secretion induced by the androgens with respect to the estrogens. It is likely that these high GH peaks and low GH troughs establish a recycling mechanism through established feedback mechanisms. That is, the high GH peak, induced by GHRH, stimulates somatostatin secretion such that a very low GH trough follows. In turn, this low GH trough, in the high somatostatin environment, establishes the correct neuroendocrine milieu for the next high GH peak, and so on. Additional studies will help clarify this model and hopefully provide a better understanding of the mechanisms regulating the interaction between gonadal steroids and GH.