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首页> 外文期刊>Endocrinology >Obestatin plays an opposite role in the regulation of pituitary somatotrope and corticotrope function in female primates and male/female mice
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Obestatin plays an opposite role in the regulation of pituitary somatotrope and corticotrope function in female primates and male/female mice

机译：Obestatin在雌性灵长类和雄性/雌性小鼠的垂体生长激素和皮质激素功能的调节中起相反的作用

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Obestatin is a 23-amino-acid amidated peptide that is encoded by the ghrelin gene. Previous studies have shown obestatin can modulate the hypothalamic neuronal circuitry that regulates pituitary function, perhaps by modulating the actions of ghrelin. However, the direct actions of obestatin on pituitary function remain controversial. Here, primary pituitary cell cultures from a nonhuman primate (baboon) and mice were used to test the effects of obestatin on pituitary hormone expression and secretion. In pituitary cultures from both species, obestatin had no effect on prolactin, LH, FSH, or TSH expression/release. Conversely, obestatin stimulated proopiomelanocortin expression and ACTH release and inhibited GH expression/release in vitro, actions that were also observed in vivo in mice treated with obestatin. In vitro, obestatin inhibited the stimulatory actions of ghrelin on GH but not ACTH release. The inhibitory effect of obestatin on somatotrope function was associated with an overall reduction in pituitary transcription factor-1 and GHRH receptor mRNA levels in vitro and in vivo as well as a reduction in hypothalamic GHRH and ghrelin expression in vivo. The stimulatory effect of obestatin on ACTH was associated with an increase in pituitary CRF receptors. Obestatin also reduced the expression of pituitary somatostatin receptors (sst1/sst2), which could serve to modify its impact on hormone secretion. The in vitro actions of obestatin on both GH and ACTH release required the adenylyl cyclase and MAPK routes. Taken together, our results provide evidence that obestatin can act directly at the pituitary to control somatotrope and corticotrope function, and these effects are conserved across species.
机译：肥胖抑制素是由生长素释放肽基因编码的23个氨基酸的酰胺化肽。先前的研究表明，肥胖抑制素可以调节下垂体神经系统的垂体功能，可能是通过调节生长素释放肽的作用来实现的。然而，肥胖抑制素对垂体功能的直接作用仍存在争议。在这里，使用来自非人类灵长类动物（狒狒）和小鼠的垂体原代细胞培养物来测试肥胖抑制素对垂体激素表达和分泌的影响。在两种物种的垂体培养物中，肥胖抑制素对催乳素，LH，FSH或TSH表达/释放均无影响。相反，肥胖抑制素在体外刺激原黑皮质素表达和ACTH释放并抑制GH表达/释放，在用肥胖抑制素治疗的小鼠体内也观察到了作用。在体外，肥胖抑制素抑制ghrelin对GH的刺激作用，但不抑制ACTH释放。肥胖抑制素对生长激素功能的抑制作用与体内外垂体转录因子-1和GHRH受体mRNA水平的总体降低以及体内下丘脑GHRH和ghrelin表达的降低有关。肥胖抑制素对促肾上腺皮质激素的刺激作用与垂体CRF受体的增加有关。 Obestatin还降低了垂体生长抑素受体（sst1 / sst2）的表达，这可能有助于改变其对激素分泌的影响。肥胖抑制素对GH和ACTH释放的体外作用需要腺苷酸环化酶和MAPK途径。综上所述，我们的结果提供了证据，表明Obestatin可以直接作用于垂体以控制生长激素和皮质激素的功能，并且这些效应在整个物种中均得到保留。

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