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肥胖的临床生物化学

The clinical biochemistry of obesity.

作者信息

Sikaris Ken A

机构信息

Melbourne Pathology, Collingwood, VIC, Australia.

出版信息

Clin Biochem Rev. 2004 Aug;25(3):165-81.

Abstract

Obesity is essentially an excessive accumulation of triacylglycerols in fatty tissue that is the net result of excessive energy intake compared to energy usage. Severe forms of the disease are most likely to have a predominantly genetic basis and this is probably polygenic. The 'thrifty gene' hypothesis also describes the disturbance that a modern environment, including higher energy intake and decreased physical activity, has on otherwise advantageous genetic variations. While the physical consequences of obesity, such as arthritis, are debilitating and costly, the metabolic consequences are the drivers behind the modern epidemics of insulin resistance, diabetes, fatty liver disease, coronary artery disease, hypertension and polycystic ovary syndrome. The pathophysiological mechanisms behind these diseases are probably a combination of the toxic metabolic effects of free fatty acids and adipokines - the numerous messengers that adipose tissue has been discovered to produce.

摘要

肥胖本质上是脂肪组织中三酰甘油的过度积累,这是能量摄入超过能量消耗的最终结果。该疾病的严重形式很可能主要基于遗传,而且可能是多基因的。“节俭基因”假说也描述了现代环境(包括能量摄入增加和体力活动减少)对原本有利的基因变异所产生的干扰。虽然肥胖的身体后果,如关节炎,会使人虚弱并造成高昂代价,但代谢后果却是现代胰岛素抵抗、糖尿病、脂肪肝疾病、冠状动脉疾病、高血压和多囊卵巢综合征流行的驱动因素。这些疾病背后的病理生理机制可能是游离脂肪酸和脂肪因子(已发现脂肪组织会产生的众多信使分子)的毒性代谢作用共同导致的。

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