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原文来源：Hypertension Volume 45, Number 6; June, 2005

我们在这篇综述里试图目的性地演绎出瘦素（Leptin）的生理学使命。因为我们目前唯一所知的引起高瘦素血症的原因是营养过度和饮食诱导的肥胖，因此我们比较了普通的瘦素化啮齿动物和非瘦素化啮齿动物营养过度的区别。对于瘦素化啮齿动物，所添加的脂质被限制在脂肪细胞中；而对于非瘦素化啮齿动物，所添加的脂质则分布在肝脏、胰腺小岛、心肌和骨骼肌中，引起器官功能紊乱及细胞死亡并伴随着一个类似于代谢综合症的疾病簇。我们在这篇综述里关注了脂质诱导的心脏功能紊乱以及高瘦素血症可预防心脏功能紊乱的显著能力。我们推断出营养过度的高瘦素血症可以通过下述两个作用来预防异位脂质堆积：（1）作用于下丘脑的食欲中心来限制热量过剩以适应现有脂肪细胞的存储容量；（2）通过对外周组织上调脂肪酸氧化并下调脂肪生成将异位脂质堆积最小化。我们对这一系统失败的原因和其临床结果进行了讨论。

Hyperleptinemia Protecting the Heart From Lipid Overload

In this review, we attempt to deduce teleologically the physiological mission of leptin. Because overnutrition and diet-induced obesity are the only known causes of hyperleptinemia, we contrast the differences in overnutrition in normally leptinized rodents, in which the added lipids are confined to adipocytes, with those of unleptinized rodents, in which the added lipids are distributed in liver, pancreatic islets, and heart and skeletal muscle, causing organ dysfunction and cell death with a disease cluster resembling metabolic syndrome. We focus here on lipid-induced cardiac dysfunction and the remarkable ability of hyperleptinemia to prevent it. We conclude that the hyperleptinemia of overnutrition prevents the ectopic lipid deposition by: (1) acting on hypothalamic appetite centers to limit the caloric surplus to fit the available adipocyte storage capacity and, (2) upregulating of fatty acid oxidation and downregulating lipogenesis in peripheral tissues to minimize ectopic lipid deposition. The causes of failure of this system and its clinical consequences are discussed.