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肥胖与代谢综合征中的交感神经系统活动。

Sympathetic system activity in obesity and metabolic syndrome.

作者信息

Tentolouris N, Liatis S, Katsilambros N

机构信息

1st Department of Propaedeutic Medicine, Athens University Medical School, 11523 Athens, Greece.

出版信息

Ann N Y Acad Sci. 2006 Nov;1083:129-52. doi: 10.1196/annals.1367.010.

Abstract

Obesity is a very common disease worldwide, resulting from a disturbance in the energy balance. The metabolic syndrome is also a cluster of abnormalities with basic characteristics being insulin resistance and visceral obesity. The major concerns of obesity and metabolic syndrome are the comorbidities, such as type 2 diabetes, cardiovascular disease, stroke, and certain types of cancers. Sympathetic nervous system (SNS) activity is associated with both energy balance and metabolic syndrome. Sympathomimetic medications decrease food intake, increase resting metabolic rate (RMR), and thermogenic responses, whereas blockage of the SNS exerts opposite effects. The contribution of the SNS to the daily energy expenditure, however, is small ( approximately 5%) in normal subjects consuming a weight maintenance diet. Fasting suppresses, whereas meal ingestion induces SNS activity. Most of the data agree that obesity is characterized by SNS predominance in the basal state and reduced SNS responsiveness after various sympathetic stimuli. Weight loss reduces SNS overactivity in obesity. Metabolic syndrome is characterized by enhanced SNS activity. Most of the indices used for the assessment of its activity are better associated with visceral fat than with total fat mass. Visceral fat is prone to lipolysis: this effect is mediated by catecholamine action on the sensitive beta(3)-adrenoceptors found in the intraabdominal fat. In addition, central fat distribution is associated with disturbances in the hypothalamo-pituitary-adrenal axis, suggesting that a disturbed axis may be implicated in the development of the metabolic syndrome. Furthermore, SNS activity induces a proinflammatory state by IL-6 production, which in turn results in an acute phase response. The increased levels of inflammatory markers seen in the metabolic syndrome may be elicited, at least in part, by SNS overactivity. Intervention studies showed that the disturbances of the autonomic nervous system seen in the metabolic syndrome are reversible.

摘要

肥胖是一种在全球范围内非常常见的疾病,由能量平衡紊乱引起。代谢综合征也是一组异常情况,其基本特征是胰岛素抵抗和内脏肥胖。肥胖和代谢综合征的主要问题是合并症,如2型糖尿病、心血管疾病、中风和某些类型的癌症。交感神经系统(SNS)活动与能量平衡和代谢综合征均有关联。拟交感神经药物可减少食物摄入、提高静息代谢率(RMR)以及产热反应,而阻断SNS则会产生相反的效果。然而,在食用维持体重饮食的正常受试者中,SNS对每日能量消耗的贡献很小(约5%)。禁食会抑制SNS活动,而进食则会诱导其活动。大多数数据表明,肥胖的特征是基础状态下SNS占主导,且在各种交感刺激后SNS反应性降低。体重减轻可降低肥胖患者的SNS过度活动。代谢综合征的特征是SNS活动增强。大多数用于评估其活动的指标与内脏脂肪的关联比与总脂肪量的关联更强。内脏脂肪易于发生脂解:这种作用是由儿茶酚胺作用于腹内脂肪中发现的敏感β(3)-肾上腺素能受体介导的。此外,中心性脂肪分布与下丘脑-垂体-肾上腺轴紊乱有关,这表明该轴的紊乱可能与代谢综合征的发生有关。此外,SNS活动通过产生白细胞介素-6诱导促炎状态,进而导致急性期反应。代谢综合征中炎症标志物水平的升高可能至少部分是由SNS过度活动引起的。干预研究表明,代谢综合征中出现的自主神经系统紊乱是可逆的。

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