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首页> 外文期刊>American Journal of Physiology >Anorectic actions of prolactin-releasing peptide are mediated by corticotropin-releasing hormone receptors.
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Anorectic actions of prolactin-releasing peptide are mediated by corticotropin-releasing hormone receptors.

机译：催乳激素释放肽的厌食作用由促肾上腺皮质激素释放激素受体介导。

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摘要

Prolactin-releasing peptide (PrRP) reduces food intake and body weight and modifies body temperature when administered centrally in rats, suggesting a role in energy homeostasis. However, the mediators of PrRP's actions are unknown. The present study, therefore, first examined the possible involvement of the anorectic neuropeptides corticotropin-releasing hormone (CRH) and the melanocortins (e.g., alpha-melanocyte-stimulating hormone) in PrRP's effects on food intake and core body temperature and, second, determined if PrRP affects energy expenditure by measuring oxygen consumption (Vo2). Intracerebroventricular injection of PrRP (4 nmol) to 24-h-fasted male Sprague-Dawley rats decreased food intake and modified body temperature. Blockade of central CRH receptors by intracerebroventricular coadministration of the CRH receptor antagonist astressin (20 microg) reversed the PrRP-induced reduction in feeding. However, astressin's effect on PrRP-induced changes in body temperature was complicated because the antagonist itself caused a slight rise in body temperature. In contrast, intracerebroventricular coadministration of the melanocortin receptor-3/4 antagonist SHU-9119 (0.1 nmol) had no effect on any of PrRP's actions. Finally, intracerebroventricular injection of PrRP (4 nmol) caused a significantly greater Vo2 over a 3-h test period compared with vehicle-treated rats. These results show that the anorectic actions of PrRP are mediated by central CRH receptors but not by melanocortin receptors-3/4 and that PrRP can modify Vo2.
机译：催乳素释放肽（PrRP）在大鼠中集中给药时可减少食物摄入量和体重，并改变体温，表明其在能量稳态中起作用。但是，PrRP行为的调解人是未知的。因此，本研究首先研究了厌食性神经肽促肾上腺皮质激素释放激素（CRH）和黑皮质素（例如，α-黑素细胞刺激激素）可能与PrRP对食物摄入和核心体温的影响有关，其次，确定了PrRP通过测量氧气消耗量（Vo2）影响能量消耗。向24小时禁食的雄性Sprague-Dawley大鼠的脑室内注射PrRP（4 nmol）会减少食物摄入并改变体温。通过脑室内共同施用CRH受体拮抗剂astressin（20微克）来阻断中央CRH受体，可以逆转PrRP诱导的进食减少。然而，由于拮抗剂本身引起体温略微升高，因此应激蛋白对PrRP诱导的体温变化的作用是复杂的。相反，黑皮质素受体-3/4拮抗剂SHU-9119（0.1 nmol）的脑室内共同给药对PrRP的任何作用均无影响。最后，与媒介物治疗的大鼠相比，在3小时的测试期内，脑室内注射PrRP（4 nmol）导致明显更大的Vo2。这些结果表明，PrRP的厌食作用是由中央CRH受体介导的，而不是由黑皮质素受体-3/4介导的，并且PrRP可以修饰Vo2。

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