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肥胖、炎症与胰岛素抵抗。

Obesity, inflammation, and insulin resistance.

作者信息

Shoelson Steven E, Herrero Laura, Naaz Afia

机构信息

Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Gastroenterology. 2007 May;132(6):2169-80. doi: 10.1053/j.gastro.2007.03.059.

DOI:10.1053/j.gastro.2007.03.059
PMID:17498510
Abstract

Weight gain and obesity are major risk factors for conditions and diseases ranging from insulin resistance and type 2 diabetes mellitus to atherosclerosis and the sequelae of nonalcoholic fatty liver disease. A chronic, subacute state of inflammation often accompanies the accumulation of excess lipid in adipose tissue and liver (hepatic steatosis), evidenced by changes in both inflammatory cells and biochemical markers of inflammation. These changes can be seen in the involved tissues and systemically, in terms of elevated circulating levels of inflammatory markers. The link between obesity and inflammation has therefore raised the important question of whether obesity-induced inflammation plays a pathogenic role in the development and progression of these disorders. We review the rapidly expanding body of animal and clinical data that support potential roles for inflammation in the pathogenesis of insulin resistance and type 2 diabetes mellitus.

摘要

体重增加和肥胖是多种病症和疾病的主要风险因素,这些病症和疾病涵盖了从胰岛素抵抗、2型糖尿病到动脉粥样硬化以及非酒精性脂肪性肝病后遗症等范围。慢性、亚急性炎症状态常伴随脂肪组织和肝脏中过量脂质的积累(肝脂肪变性),这可通过炎症细胞和炎症生化标志物的变化得到证明。这些变化在受累组织以及全身都能看到,表现为循环炎症标志物水平升高。因此,肥胖与炎症之间的联系引发了一个重要问题,即肥胖诱导的炎症在这些疾病的发生和发展中是否起致病作用。我们回顾了迅速增长的动物和临床数据,这些数据支持炎症在胰岛素抵抗和2型糖尿病发病机制中的潜在作用。

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