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非酒精性脂肪性肝病与2型糖尿病:共同的病理生理机制

Nonalcoholic fatty liver disease and type 2 diabetes: common pathophysiologic mechanisms.

作者信息

Saponaro Chiara, Gaggini Melania, Gastaldelli Amalia

机构信息

Cardiometabolic Risk Unit, Institute of Clinical Physiology, CNR, via Moruzzi 1, 56100, Pisa, Italy,

出版信息

Curr Diab Rep. 2015 Jun;15(6):607. doi: 10.1007/s11892-015-0607-4.

Abstract

Nonalcoholic fatty liver disease (NAFLD) is an independent risk factor for advanced liver disease, type 2 diabetes (T2DM), and cardiovascular diseases. The prevalence of NAFLD in the general population is around 30 %, but it is up to three times higher in those with T2DM. Among people with obesity and T2DM, the NAFLD epidemic also is worsening. Therefore, it is important to identify early metabolic alterations and to prevent these diseases and their progression. In this review, we analyze the pathophysiologic mechanisms leading to NAFLD, particularly, those common to T2DM, such as liver and muscle insulin resistance. However, it is mainly adipose tissue insulin resistance that results in increased hepatic de novo lipogenesis, inflammation, and lipotoxicity. Although genetics predispose to NAFLD, an unhealthy lifestyle, including high-fat/high-sugar diets and low physical activity, increases the risk. In addition, alterations in gut microbiota and environmental chemical agents, acting as endocrine disruptors, may play a role.

摘要

非酒精性脂肪性肝病(NAFLD)是晚期肝病、2型糖尿病(T2DM)和心血管疾病的独立危险因素。普通人群中NAFLD的患病率约为30%,但在T2DM患者中患病率高达三倍。在肥胖和T2DM患者中,NAFLD的流行情况也在恶化。因此,识别早期代谢改变并预防这些疾病及其进展非常重要。在本综述中,我们分析了导致NAFLD的病理生理机制,特别是那些与T2DM共有的机制,如肝脏和肌肉胰岛素抵抗。然而,主要是脂肪组织胰岛素抵抗导致肝脏从头脂肪生成增加、炎症和脂毒性。尽管遗传因素易患NAFLD,但不健康的生活方式,包括高脂肪/高糖饮食和低体力活动,会增加患病风险。此外,肠道微生物群的改变和作为内分泌干扰物的环境化学物质可能也起作用。

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