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低脂联素血症:内脏肥胖与代谢综合征之间的联系。

Hypoadiponectinemia: A Link between Visceral Obesity and Metabolic Syndrome.

作者信息

Di Chiara Tiziana, Argano Christiano, Corrao Salvatore, Scaglione Rosario, Licata Giuseppe

机构信息

Dipartimento Biomedico di Medicina Interna e Specialistica, Università Degli Studi di Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy.

出版信息

J Nutr Metab. 2012;2012:175245. doi: 10.1155/2012/175245. Epub 2011 Oct 16.

DOI:10.1155/2012/175245
PMID:22013516
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3195429/
Abstract

Metabolic syndrome (MetS) represents a combination of cardiometabolic risk factors, including visceral obesity, glucose intolerance or type 2 diabetes, elevated triglycerides, reduced HDL cholesterol, and hypertension. MetS is rapidly increasing in prevalence worldwide as a consequence of the "epidemic" obesity, with a considerable impact on the global incidence of cardiovascular disease and type 2 diabetes. At present, there is a growing interest on the role of visceral fat accumulation in the occurrence of MetS. In this review, the effects of adipocytokines and other proinflammatory factors produced by fat accumulation on the occurrence of the MetS have been also emphasized. Accordingly, the "hypoadiponectinemia" has been proposed as the most interesting new hypothesis to explain the pathophysiology of MetS.

摘要

代谢综合征(MetS)是多种心血管代谢危险因素的组合,包括内脏肥胖、葡萄糖耐量异常或2型糖尿病、甘油三酯升高、高密度脂蛋白胆固醇降低以及高血压。由于“流行”性肥胖,MetS在全球的患病率正在迅速上升,对全球心血管疾病和2型糖尿病的发病率产生了相当大的影响。目前,人们越来越关注内脏脂肪堆积在MetS发生中的作用。在这篇综述中,还强调了脂肪堆积产生的脂肪细胞因子和其他促炎因子对MetS发生的影响。因此,“低脂联素血症”已被提出作为解释MetS病理生理学的最有趣的新假说。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/3195429/a1d2a62391d8/JNUME2012-175245.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/3195429/7fb87f7ba911/JNUME2012-175245.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/3195429/a1d2a62391d8/JNUME2012-175245.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/3195429/7fb87f7ba911/JNUME2012-175245.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/3195429/a1d2a62391d8/JNUME2012-175245.002.jpg

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