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瘦素在肥胖相关性高血压中的作用。

Role of leptin in obesity-related hypertension.

作者信息

Haynes William G

机构信息

General Clinical Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.

出版信息

Exp Physiol. 2005 Sep;90(5):683-8. doi: 10.1113/expphysiol.2005.031237. Epub 2005 Aug 16.

Abstract

Obesity in humans causes hypertension, myocardial hypertrophy and coronary atherosclerosis, and increased cardiovascular morbidity and mortality that is thought to be related to sympathetic overactivity. Leptin is an adipocyte-derived hormone that acts in the hypothalamus to regulate appetite, energy expenditure and sympathetic nervous system outflow. One of the major mechanisms leading to the development of obesity-induced hypertension appears to be leptin-mediated sympatho-activation. Leptin adversely shifts the renal pressure-natriuresis curve, leading to relative sodium retention. Although obesity is generally associated with resistance to the anorexic and weight-reducing actions of leptin, our work has shown preservation of its sympatho-excitatory and pressor actions. This selective leptin resistance of obesity, coupled with hyperleptinaemia, may play a critical role in the cardiovascular complications of obesity. Increased information about leptin and its mechanisms of actions should help the development of safe and effective pharmacological treatments of obesity and obesity-related hypertension.

摘要

人类肥胖会导致高血压、心肌肥大和冠状动脉粥样硬化,并增加心血管疾病的发病率和死亡率,这被认为与交感神经过度活跃有关。瘦素是一种由脂肪细胞产生的激素,作用于下丘脑,调节食欲、能量消耗和交感神经系统输出。导致肥胖诱导型高血压发展的主要机制之一似乎是瘦素介导的交感神经激活。瘦素会不利地改变肾压力-利钠曲线,导致相对钠潴留。虽然肥胖通常与对瘦素的厌食和减重作用产生抵抗有关,但我们的研究表明其交感神经兴奋作用和升压作用得以保留。肥胖这种选择性的瘦素抵抗,再加上高瘦素血症,可能在肥胖的心血管并发症中起关键作用。关于瘦素及其作用机制的更多信息,应有助于开发安全有效的肥胖及肥胖相关高血压的药物治疗方法。

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