Regulation of gonadotropin secretion by monitoring energy availability

Abstract

Nutrition is a principal environmental factor influencing fertility in animals. Energy deficit causes amenorrhea, delayed puberty, and suppression of copulatory behaviors by inhibiting gonadal activity. When gonadal activity is impaired by malnutrition, the signals originating from an undernourished state are ultimately conveyed to the gonadotropin-releasing hormone (GnRH) pulse generator, leading to suppressed secretion of GnRH and luteinizing hormone (LH). The mechanism responsible for energetic control of gonadotropin release is believed to involve metabolic signals, sensing mechanisms, and neuroendocrine pathways. The availabilities of blood-borne energy substrates such as glucose, fatty acids, and ketone bodies, which fluctuate in parallel with changes in nutritional status, act as metabolic signals that regulate the GnRH pulse generator activity and GnRH/LH release. As components of the specific sensing system, the ependymocytes lining the cerebroventricular wall in the lower brainstem integrate the information derived from metabolic signals to control gonadotropin release. One of the pathways responsible for the energetic control of gonadal activity consists of noradrenergic neurons from the solitary tract nucleus in the lower brainstem, projecting to the paraventricular nucleus of the hypothalamus. Further studies are needed to elucidate the mechanisms underlying energetic control of reproductive function.

Investigating pleiotropic effects of statins on ischemic heart disease in the UK Biobank using Mendelian randomisation

“…Notably, upregulation of indicators of plentiful living conditions, such as insulin, appear to cause IHD, particularly in men ( Zhao et al, 2019 ), likely via gonadotropin releasing hormone (GnRH) ( Schooling and Ng, 2019 ). Similarly, fatty acids may affect GnRH ( Tran et al, 2016 ; Matsuyama and Kimura, 2015 ). In contrast, indicators of adversity, such as endotoxins promote an inflammatory response, involving interleukins, which suppresses the reproductive axis ( Kalra et al, 1998 ) and thereby testosterone ( Tremellen et al, 2018 ), which may be reversed by anakinra possibly outweighing the benefits for IHD of suppressing inflammation ( Tardif et al, 2019 ).…”

Potential functional variants in AHR signaling pathways are associated with age at puberty in swine

“…Puberty in gilts is attained by a reduction of estrogen inhibition of the GnRH pulse generator, allowing increased LH pulses which leads to the onset of cyclicity (Lents et al 2020) and is dependent upon ovarian follicular development, which can be affected by boar exposure, stress, feed or energy intake and growth rate (Zhuo et al 2014;Matsuyama & Kimura 2014;Knox 2019). It is reported here that season in which a gilt is born has a significant effect on the age at which she reaches puberty.…”

Pleiotropic effects of statins on ischemic heart disease: a Mendelian Randomization study in the UK Biobank

“…Notably, upregulation of indicators of plentiful living conditions, such as insulin, appear to cause IHD, particularly in men [49], likely via gonadotropin releasing hormone (GnRH) [48]. Similarly, fatty acids may affect GnRH [50, 51]. In contrast, indicators of adversity, such as endotoxins promote an inflammatory response, involving interleukins, which suppresses the reproductive axis [52] and thereby testosterone [53], which may be reversed by anakinra possibly outweighing the benefits for IHD of suppressing inflammation [54].…”