Wahab F, Shahab M, Behr R
Stem Cell Biology Unit Leibniz Institute for Primate Research, German Primate Center, Kellnerweg 4, D-37077 Göttingen, Germany Laboratory of Reproductive Neuroendocrinology Department of Animal Sciences, Faculty of Biological Sciences, Quiad-i-Azam University, Islamabad, Pakistan.
Stem Cell Biology Unit Leibniz Institute for Primate Research, German Primate Center, Kellnerweg 4, D-37077 Göttingen, Germany Laboratory of Reproductive Neuroendocrinology Department of Animal Sciences, Faculty of Biological Sciences, Quiad-i-Azam University, Islamabad, Pakistan
J Endocrinol. 2015 May;225(2):R49-66. doi: 10.1530/JOE-14-0688.
Recently, kisspeptin (KP) and gonadotropin inhibitory hormone (GnIH), two counteracting neuropeptides, have been acknowledged as significant regulators of reproductive function. KP stimulates reproduction while GnIH inhibits it. These two neuropeptides seem to be pivotal for the modulation of reproductive activity in response to internal and external cues. It is well-documented that the current metabolic status of the body is closely linked to its reproductive output. However, how reproductive function is regulated by the body's energy status is less clear. Recent studies have suggested an active participation of hypothalamic KP and GnIH in the modulation of reproductive function according to available metabolic cues. Expression of KISS1, the KP encoding gene, is decreased while expression of RFRP (NPVF), the gene encoding GnIH, is increased in metabolic deficiency conditions. The lower levels of KP, as suggested by a decrease in KISS1 gene mRNA expression, during metabolic deficiency can be corrected by administration of exogenous KP, which leads to an increase in reproductive hormone levels. Likewise, administration of RF9, a GnIH receptor antagonist, can reverse the inhibitory effect of fasting on testosterone in monkeys. Together, it is likely that the integrated function of both these hypothalamic neuropeptides works as a reproductive output regulator in response to a change in metabolic status. In this review, we have summarized literature from nonprimate and primate studies that demonstrate the involvement of KP and GnIH in the metabolic regulation of reproduction.
最近，促性腺激素释放激素（KP）和促性腺激素抑制激素（GnIH）这两种起相反作用的神经肽，已被公认为生殖功能的重要调节因子。KP刺激生殖，而GnIH抑制生殖。这两种神经肽似乎对于响应内部和外部线索调节生殖活动至关重要。有充分的文献记载，身体当前的代谢状态与其生殖产出密切相关。然而，身体的能量状态如何调节生殖功能尚不清楚。最近的研究表明，下丘脑的KP和GnIH根据可用的代谢线索积极参与生殖功能的调节。在代谢不足的情况下，编码KP的基因KISS1的表达降低，而编码GnIH的基因RFRP（NPVF）的表达增加。代谢不足期间，如KISS1基因mRNA表达降低所表明的，KP水平较低，可通过给予外源性KP来纠正，这会导致生殖激素水平升高。同样，给予GnIH受体拮抗剂RF9可以逆转禁食对猴子睾酮的抑制作用。总之，这两种下丘脑神经肽的综合功能可能作为生殖产出调节因子，以响应代谢状态的变化。在这篇综述中，我们总结了来自非灵长类和灵长类研究的文献，这些文献证明了KP和GnIH参与生殖的代谢调节。
