Popovic V, Duntas L H
Neuroendocrine Unit, Institute of Endocrinology, University Clinical Center, Belgrade, Serbia.
Horm Metab Res. 2005 Sep;37(9):533-7. doi: 10.1055/s-2005-870418.
The hypothalamus has long been recognized as a major site in the central nervous system (CNS) where a spectrum of internal and external environmental information is integrated for energy homeostasis. The isolation and sequencing of leptin in the mid 90 s, together with the demonstration of leptin administration's ability to correct the obesity syndrome in leptin-deficient ob/ob mice and humans by suppressing food intake and weight gain in laboratory rodents, confirmed the hypothesized existence of a direct humoral signal from adipose tissue to the hypothalamus, thus integrating the energy-related signals. In the 80 s, neuropeptide Y (NPY) was identified as a potent appetite-stimulating neuropeptide produced, released and acting locally within the hypothalamus. This is recognized as a major physiological appetite transducer and central neurochemical substrate receiving, interpreting and processing incoming information on energy status. More recently, ghrelin, produced in the stomach and released into the general circulation, has drawn attention as the other limb of the feedback circuit that stimulates appetite at NPY network level. Prolonged fasting suppresses serum leptin, while suppressing TSH secretion. Intervention with leptin replacement can prevent fasting-induced changes in TSH, suggesting that leptin regulates TSH. Low leptin levels in sportsmen and sportswomen as well as in recreational runners are consistent with reduction in body fat, but are also influenced by the presence of low insulin, hypothyroxemia, and elevated cortisol levels. These metabolic adaptations to chronic energy deficits indicate a role in leptin regulation. A study within the general population found that activity levels and leptin were significantly negatively associated in both sexes. Circulating ghrelin levels, however, do not change during energy expenditure.
长期以来，下丘脑一直被认为是中枢神经系统（CNS）中的一个主要部位，在这里，一系列内部和外部环境信息被整合以维持能量平衡。20世纪90年代中期瘦素的分离和测序，以及通过抑制实验室啮齿动物的食物摄入和体重增加来证明给予瘦素能够纠正瘦素缺乏的ob/ob小鼠和人类的肥胖综合征，证实了从脂肪组织到下丘脑存在直接体液信号的假设，从而整合了与能量相关的信号。在20世纪80年代，神经肽Y（NPY）被确定为一种在下丘脑中产生、释放并在局部起作用的强效食欲刺激神经肽。这被认为是一种主要的生理食欲传感器和中枢神经化学底物，接收、解释和处理有关能量状态的传入信息。最近，胃中产生并释放到全身循环中的胃饥饿素，作为反馈回路的另一部分引起了关注，它在NPY网络水平上刺激食欲。长期禁食会抑制血清瘦素，同时抑制促甲状腺激素（TSH）分泌。用瘦素替代进行干预可以预防禁食引起的TSH变化，表明瘦素调节TSH。男性和女性运动员以及业余跑步者的瘦素水平较低，这与体脂减少一致，但也受到低胰岛素、低甲状腺素血症和皮质醇水平升高的影响。这些对慢性能量不足的代谢适应表明瘦素调节中存在作用。一项针对普通人群的研究发现，活动水平和瘦素在两性中均呈显著负相关。然而，在能量消耗期间，循环中的胃饥饿素水平不会改变。
