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Prepro-orexin and feeding-related peptide receptor expression in dehydration-induced anorexia.

机译:脱水诱导的厌食症中的前原毒素和与进食相关的肽受体表达。

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Food-restricted animals present metabolic adaptations that facilitate food-seeking behavior and decelerate energy utilization by reducing the hypothalamus-pituitary-thyroid (HPT) axis function. Stress by dehydration induces an anorexic behavior in rats, loss of weight and reduced food intake when compared to ad libitum fed animals, however these alterations are accompanied by HPT axis changes such as increased serum thyrotropin levels and enhanced expression of thyrotropin-releasing hormone (TRH) in the paraventricular nucleus of the hypothalamus, which is considered as anorexigenic peptide. In contrast, a pair-fed group conformed by forced-food-restricted animals (FFR) (eating the exact same amount of food as dehydration-induced anorexic rats--DIA rats) present decreased TRH mRNA levels. NPY synthesis in the arcuate nucleus and orexin-expressing neurons from the lateral hypothalamic area (LHA) are activated during food restriction. These brain structures project into PVN, suggesting that NPY and orexins are possible factors involved in TRHergic neuron activation in DIA rats. Leptin signaling is another likely factor to be involved in TRH differential expression. Therefore, to gain more insight into the regulation of the feeding behavior in the experimental models, we analyzed Y1, Y5, Ox1-R and Ob-R(b) mRNA levels in PVN and prepro-orexin in LHA, since their signaling to the PVN might be altering TRH synthesis and feeding in DIA animals. Prepro-orexinergic cells were activated in FFR animals; Ox1-R and Y1 expression was reduced in FFR vs. controls or DIA group. Compensatory changes in PVN receptor expression of some feeding-related peptides in anorexic rats may alter TRHergic neural response to energy demands.
机译:限制食物的动物具有新陈代谢适应功能,通过降低下丘脑-垂体-甲状腺(HPT)轴功能来促进觅食行为并降低能量利用。与随意喂养的动物相比,脱水引起的应激会诱发大鼠厌食症,体重减轻和食物摄入减少,但是这些改变会伴随HPT轴变化,例如血清促甲状腺激素水平升高和促甲状腺激素释放激素(TRH)表达增强)在下丘脑的室旁核中,这被认为是致厌食性肽。相比之下,一对由强迫食物限制动物(FFR)组成的成对喂养组(与脱水诱导的厌食症大鼠(DIA大鼠)吃的食物量完全相同)的TRH mRNA水平降低。食物限制期间,弓形核中的NPY合成和来自下丘脑外侧(LHA)的食欲素表达神经元被激活。这些大脑结构投射到PVN中,表明NPY和食欲素可能是DIA大鼠TRH能神经元激活的相关因素。瘦素信号传导是TRH差异表达中另一个可能的因素。因此,为了更深入地了解实验模型中进食行为的调节,我们分析了PVN中的Y1,Y5,Ox1-R和Ob-R(b)mRNA水平以及LHA中的前原毒素,因为它们通过信号传导PVN可能正在改变DIA动物的TRH合成和喂养。前促肾上腺素能细胞在FFR动物中被激活。与对照组或DIA组相比,FFR的Ox1-R和Y1表达降低。厌食症大鼠中一些与进食相关的肽的PVN受体表达的代偿性改变可能会改变TRH能神经对能量需求的反应。

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