Animals have developed highly adaptive and redundant mechanisms to maintain energy balance by matching caloric intake to caloric expenditure. Recent evidence has pointed to a variety of peripheral signals that inform specific central nervous system (CNS) circuits about the status of peripheral energy stores as critical to the maintenance of energy balance. A critical component of these CNS circuits is the melanocortin system. Regulation of signaling by melanocortin 3 and melanocortin 4 receptors in the CNS is controlled via neuronal cell bodies in the arcuate nucleus of the hypothalamus that synthesize melanocortin receptor agonists such as alpha-melanocyte-stimulating hormone (alpha-MSH) or antagonists such as agouti-related protein (AgRP). The activity of these two populations of neurons is reciprocally regulated by a number of peripheral and central systems that influence energy balance. Further, increased melanocortin signaling via pharmacological or genetic means in the CNS causes potent reductions in food intake and weight loss. Decreased melanocortin signaling via pharmacological or genetic means results in increased food intake and weight gain. Reviewed here is the wide range of evidence that points to the melanocortin system as a critical node in the diverse neurocircuitry that regulates food intake and body weight.

中文翻译：

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黑皮质素系统在控制能量平衡中的关键作用。

动物已经开发出高度适应性和冗余机制，通过将热量摄入与热量消耗相匹配来维持能量平衡。最近的证据指向各种外围信号，这些信号通知特定的中枢神经系统（CNS）电路有关外围能量存储状态的信息，这对于维持能量平衡至关重要。这些中枢神经系统电路的关键组件是黑皮质素系统。中枢神经系统中黑皮质素3和黑皮质素4受体对信号传导的调节是通过下丘脑弓状核中的神经元细胞体来控制的，该神经元细胞合成黑皮质素受体激动剂，例如α-黑素细胞刺激激素（α-MSH）或拮抗剂，例如刺鼠相关蛋白（AgRP）。这两个神经元群体的活动受到许多影响能量平衡的外围和中央系统的相互调节。此外，中枢神经系统中通过药理或遗传手段增加的黑皮质素信号传导导致食物摄入和体重减轻的有效减少。通过药理或遗传手段降低黑皮质素信号传导会导致食物摄入增加和体重增加。本文复习了广泛的证据，这些证据表明黑皮质素系统是调节食物摄入和体重的各种神经回路中的关键节点。通过药理或遗传手段降低黑皮质素信号传导会导致食物摄入增加和体重增加。本文复习了广泛的证据，这些证据表明黑皮质素系统是调节食物摄入和体重的各种神经回路中的关键节点。通过药理或遗传手段降低黑皮质素信号传导会导致食物摄入增加和体重增加。本文复习了广泛的证据，这些证据表明黑皮质素系统是调节食物摄入和体重的各种神经回路中的关键节点。