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[肥胖的分子原理]

[Molecular principles of obesity].

作者信息

Hamann A, Münzberg H, Algenstaedt P, Tafel J

机构信息

Abteilung Innere Medizin I, Medizinische Klinik und Poliklinik der Universität Heidelberg.

出版信息

Herz. 2001 May;26(3):178-84. doi: 10.1007/pl00002020.

Abstract

BACKGROUND

The deposition of excess amounts of energy in adipose tissue is enhanced by high-fat diets and lack of physical activity. Furthermore, the existence of a specific genetic predisposition towards the development of obesity becomes evident by marked interindividual differences in the response to caloric oversupply.

GENETIC DEFECTS AND HORMONES

In recent years, numerous genes and genetic defects with importance for human obesity were identified, especially through studies in animal models. The adipocyte-derived hormone leptin and its hypothalamic receptor play a premier role, as they interact with a network of proteins and neuropeptides within the regulation of food intake and energy expenditure.

CONCLUSION

The search for the key molecular mechanisms in the pathogenesis of obesity will not only improve our understanding of energy metabolism, but may ultimately also lead to the development of new treatment strategies for obese patients.

摘要

背景

高脂肪饮食和缺乏体育活动会加剧脂肪组织中过量能量的沉积。此外,对热量供应过多的反应存在明显的个体差异,这表明存在导致肥胖的特定遗传易感性。

遗传缺陷与激素

近年来,尤其是通过动物模型研究,发现了许多对人类肥胖具有重要意义的基因和遗传缺陷。脂肪细胞衍生的激素瘦素及其下丘脑受体起着首要作用,因为它们在食物摄入和能量消耗的调节中与蛋白质和神经肽网络相互作用。

结论

寻找肥胖发病机制中的关键分子机制不仅会增进我们对能量代谢的理解,而且最终可能还会促成针对肥胖患者的新治疗策略的开发。

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