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首页> 外文期刊>Frontiers in neuroendocrinology >Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance.
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Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance.

机译：下丘脑中的瘦素信号传导：强调能量稳态和瘦素抵抗。

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Leptin, the long-sought satiety factor of adipocytes origin, has emerged as one of the major signals that relay the status of fat stores to the hypothalamus and plays a significant role in energy homeostasis. Understanding the mechanisms of leptin signaling in the hypothalamus during normal and pathological conditions, such as obesity, has been the subject of intensive research during the last decade. It is now established that leptin action in the hypothalamus in regulation of food intake and body weight is mediated by a neural circuitry comprising of orexigenic and anorectic signals, including NPY, MCH, galanin, orexin, GALP, alpha-MSH, NT, and CRH. In addition to the conventional JAK2-STAT3 pathway, it has become evident that PI3K-PDE3B-cAMP pathway plays a critical role in leptin signaling in the hypothalamus. It is now established that central leptin resistance contributes to the development of diet-induced obesity and ageing associated obesity. Central leptin resistance also occurs due to hyperleptinimia produced by exogenous leptin infusion. A defective nutritional regulation of leptin receptor gene expression and reduced STAT3 signaling may be involved in the development of leptin resistance in DIO. However, leptin resistance in the hypothalamic neurons may occur despite an intact JAK2-STAT3 pathway of leptin signaling. Thus, in addition to defective JAK2-STAT3 pathway, defects in other leptin signaling pathways may be involved in leptin resistance. We hypothesize that defective regulation of PI3K-PDE3B-cAMP pathway may be one of the mechanisms behind the development of central leptin resistance seen in obesity.
机译：瘦素是脂肪细胞起源的长期饱腹感因子，已成为将脂肪储存状态传递到下丘脑的主要信号之一，并在能量稳态中发挥重要作用。在过去的十年中，了解正常和病理状态（例如肥胖症）下丘脑中瘦素信号传导的机制一直是深入研究的主题。现在已经确定，下丘脑中瘦素在调节食物摄入和体重中的作用是由神经系统介导的，所述神经系统包括致畸和厌食信号，包括NPY，MCH，甘丙肽，食欲肽，GALP，α-MSH，NT和CRH 。除常规的JAK2-STAT3途径外，很明显PI3K-PDE3B-cAMP途径在下丘脑的瘦素信号传导中起关键作用。现在已经确定，中央瘦素​​抵抗性有助于饮食诱导的肥胖症和与衰老相关的肥胖症的发展。中央瘦素抵抗也由于外源性瘦素输注产生的高瘦素而发生。瘦素受体基因表达的营养调节不良和STAT3信号转导减少可能与DIO中瘦素抵抗的发展有关。然而，尽管瘦素信号传导的JAK2-STAT3通路完整，下丘脑神经元中仍可能发生瘦素抵抗。因此，除了有缺陷的JAK2-STAT3途径，其他瘦素信号传导途径的缺陷也可能与瘦素抗性有关。我们假设PI3K-PDE3B-cAMP途径的调控不完善可能是肥胖中见到的中央瘦素抵抗发展的机制之一。

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