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Erschienen in: Reproductive Medicine and Biology 2/2015

01.04.2015 | Review Article

Regulation of gonadotropin secretion by monitoring energy availability

verfasst von: Shuichi Matsuyama, Koji Kimura

Erschienen in: Reproductive Medicine and Biology | Ausgabe 2/2015

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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.
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Metadaten
Titel
Regulation of gonadotropin secretion by monitoring energy availability
verfasst von
Shuichi Matsuyama
Koji Kimura
Publikationsdatum
01.04.2015
Verlag
Springer Japan
Erschienen in
Reproductive Medicine and Biology / Ausgabe 2/2015
Print ISSN: 1445-5781
Elektronische ISSN: 1447-0578
DOI
https://doi.org/10.1007/s12522-014-0194-0

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