Signal Transduction Pathways for Leptin
Signal Transduction Pathways for Leptin
复制标题
瘦素的信号转导途径
作者：
S. Chua
瘦素是哺乳动物能量平衡的关键调节剂，并已成为无数研究食物摄入和能量消耗调节的起点（1）。在高生理浓度下，瘦素导致食物摄入减少，能量消耗增加，并转变为脂肪酸氧化增加。这些生理变化导致体重和体脂含量降低。相反，缺乏瘦素导致肥胖，这是由于食欲过盛和脂肪生成增加。在瘦素信号传导缺陷中，棕色脂肪组织，小型啮齿动物中的主要产热器官，由于交感神经系统活动减少而失去其产热能力。在本期《糖尿病》中，Rahmouni等人（2）提出了一种新的分子机制，瘦素通过这种机制刺激啮齿动物的厌食和产热反应。
考虑到瘦素在能量平衡方面的大部分作用发生在中枢神经系统内，目前公认的是，下丘脑内的瘦素受体神经元的分布式网络负责介导对脂肪组织内能量储存波动的协调反应（3）。携带瘦素受体的神经元是...
Leptin is a critical regulator of energy balance in mammals and has served as a launch point for innumerable studies examining the regulation of food intake and energy expenditure (1). At high physiological concentrations, leptin causes a decrease in food intake, an increase in energy expenditure, and a shift to increased fatty acid oxidation. These physiological shifts lead to a decrease in body weight and body fat content. Conversely, a lack of leptin leads to obesity due to hyperphagia and increased lipogenesis. In leptin signaling deficiencies, brown adipose tissue, a major thermogenic organ in small rodents, loses its thermogenic capacity due to diminished sympathetic nervous system activity. In this issue of Diabetes , Rahmouni et al. (2) present a new molecular mechanism by which leptin stimulates anorectic and thermogenic responses in rodents.
Given that most of leptin's actions with regard to energy balance occur within the central nervous system, it is currently accepted that a distributed network of leptin receptor–bearing neurons within the hypothalamus are responsible for mediating a concerted response to fluctuations of energy stores within adipose tissue (3). Leptin receptor–bearing neurons are …