Nonalcoholic Fatty Liver Disease and Type 2 Diabetes: Common Pathophysiologic Mechanisms
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  • 作者:Chiara Saponaro ; Melania Gaggini ; Amalia Gastaldelli
  • 关键词:Fatty liver ; Glucose intolerance ; De novo lipogenesis ; Lipotoxicity ; Gut microbiota ; Endocrine disruptors ; NASH
  • 刊名:Current Diabetes Reports
  • 出版年:2015
  • 出版时间:June 2015
  • 年:2015
  • 卷:15
  • 期:6
  • 全文大小:647 KB
  • 参考文献:Papers of particular interest, published recently, have been highlighted as: -Of importance ?-Of major importance1.Whiting DR, Guariguata L, Weil C, Shaw J. IDF diabetes atlas: global estimates of the prevalence of diabetes for 2011 and 2030. Diabetes Res Clin Pract. 2011;94:311-1.PubMed
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  • 作者单位:Chiara Saponaro (1) (2)
    Melania Gaggini (1) (3)
    Amalia Gastaldelli (1)

    1. Cardiometabolic Risk Unit, Institute of Clinical Physiology, CNR, via Moruzzi 1, 56100, Pisa, Italy
    2. Dipartimento di Biotecnologie, Chimica e Farmacia, Università di Siena, Siena, Italy
    3. Dipartimento di Patologia Chirurgica, Molecolare Medica e di Area Critica, Università di Pisa, Pisa, Italy
  • 刊物主题:Diabetes;
  • 出版者:Springer US
  • ISSN:1539-0829
文摘
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.

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