Relationships of adrenoceptor polymorphisms with obesity.

Relationships of adrenoceptor polymorphisms with obesity.
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DOI:
10.1155/2011/609485
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发表时间:
2011
期刊:
影响因子:
3.3
通讯作者:
Lambert GW
Lambert GW
中科院分区:
其他
文献类型:
--
作者:
Masuo K;Lambert GW

文献摘要

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肥胖、高血压和2型糖尿病是日益严重的公共卫生问题。交感神经活动增强是肥胖症、高血压和2型糖尿病的常见现象。人类肥胖、高血压和糖尿病有很强的遗传和环境决定因素。能量消耗减少和静息代谢率是体重增加的预测因素,交感神经系统通过产热参与调节能量平衡。儿茶酚胺在肥胖中的生热作用主要是通过人类的β2和β3肾上腺素能受体介导的。此外,β2肾上腺素受体对血管反应性有重要影响,并可能调节血压。β受体基因多态性也与肾上腺素受体脱敏、肥胖症增加、胰岛素抵抗和交感神经活性增强有关。许多流行病学研究表明,肾上腺素能受体基因多态性与肥胖之间存在很强的联系,但观察结果并不一致。本文将就交感神经系统和β2和β3肾上腺素能受体基因多态性在肥胖中的影响进行讨论。
Obesity, hypertension, and type 2 diabetes are rapidly growing public health problems. Heightened sympathetic nerve activity is a well-established observation in obesity, hypertension, and type 2 diabetes. Human obesity, hypertension, and diabetes have strong genetic as well as environmental determinants. Reduced energy expenditure and resting metabolic rate are predictive of weight gain, and the sympathetic nervous system participates in regulating energy balance through thermogenesis. The thermogenic effects of catecholamines in obesity are mainly mediated via the β2, and β3-adrenergic receptors in humans. Further, β2-adrenoceptors importantly influence vascular reactivity and may regulate blood pressure. β-adrenoceptor polymorphisms have also been associated with adrenoceptor desensitization, increased adiposity, insulin resistance, and enhanced sympathetic nervous activity. Many epidemiological studies have shown strong relationships between adrenoceptor polymorphisms and obesity, but the observations have been discordant. This paper will discuss the current topics involving the influence of the sympathetic nervous system and β2- and β3-adrenoceptor polymorphisms in obesity.