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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Peptide signals regulating food intake and energy homeostasis.
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Peptide signals regulating food intake and energy homeostasis.

机译：肽信号调节食物摄入和能量稳态。

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摘要

The adiposity hormone leptin has been shown to decrease food intake and body weight by acting on neuropeptide circuits in the hypothalamus. However, it is not clear how this primary hypothalamic action of leptin is translated into a change in food intake. We hypothesize that the behavioral effect of leptin ultimately involves the integration of neuronal responses in the forebrain with those in the nucleus tractus solitarius in the caudal brainstem, where ingestive behavior signals are received from the gastrointestinal system and the blood. One example is the peptide cholecystokinin, which is released from the gut following ingestion of a meal and acts via vagal afferent nerve fibers to activate medial nucleus tractus solitarius neurons and thereby decrease meal size. While it is established that leptin acts in the arcuate nucleus in the hypothalamus to stimulate anorexigenic neurons that inhibit food intake while simulataneously inhibiting orexigenic neurons that increase food intake, the mechanisms linking these effects with regions of the caudal brainstem that integrate cues related to meal termination are unclear. Based on an increasing body of supportive data, we hypothesize that this integration involves a pathway comprising descending projections from neurons from the paraventricular nucleus to neurons within the nucleus tractus solitarius that are activated by meal-related satiety factors. Leptin's anorexic effect comprises primarily decreased meal size, and at subthreshold doses for eliciting an effect on food intake, leptin intensifies the satiety response to circulating cholecystokinin. The location of neurons subserving the effects of intracerebroventricular administration of leptin and intraperitoneal injection of cholecystokinin on food intake has been identified by analysis of Fos expression. These studies reveal a distribution that includes the paraventricular nucleus and regions within the caudal brainstem, with the medial nucleus tractus solitarius having the most pronounced Fos expression in response to leptin and cholecystokinin, and support the hypothesis that the long-term adiposity signal leptin and the short-term satiety signal cholecystokinin act in concert to maintain body weight homeostasis.
机译：肥胖激素瘦素已被证明通过作用于下丘脑的神经肽回路而减少食物摄入和体重。但是，尚不清楚这种瘦素的主要下丘脑作用如何转化为食物摄入的变化。我们假设瘦素的行为作用最终涉及前脑神经元反应与尾脑干中孤索核中神经元反应的整合，在那里从胃肠系统和血液中接收到食性信号。一个例子是肽胆囊收缩素，它在进餐后从肠中释放出来，并通过迷走神经传入神经纤维起作用，以激活孤束腹内侧神经元，从而减小进餐量。虽然已经确定瘦素在下丘脑的弓形核中起作用，以刺激抑制食物摄取的厌食神经元，同时抑制增加食物摄取的食源性神经元，但这些机制与尾部脑干区域相关，这些区域整合了与进餐终止有关的线索还不清楚。基于越来越多的支持数据，我们假设这种整合涉及一条路径，该路径包括从进餐相关饱食因子激活的神经元从室旁核到孤束核内神经元的递减投影。瘦素的厌食作用主要包括减少进餐量，在低于阈值的剂量下引起对食物摄入的影响，瘦素会增强对循环性胆囊收缩素的饱腹感。通过对Fos表达的分析已经确定了维持脑室内施用瘦素和腹膜内注射胆囊收缩素对食物摄取影响的神经元的位置。这些研究揭示了包括脑室旁核和尾脑干内区域的分布，其中孤束中核对瘦素和胆囊收缩素有最明显的Fos表达，并支持长期肥胖信号瘦素和短期饱食感信号使胆囊收缩素协同作用，以维持体重的体内平衡。

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