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非酒精性脂肪性肝病对加速代谢并发症的影响。

Impact of non-alcoholic fatty liver disease on accelerated metabolic complications.

作者信息

Fan Jian Gao

机构信息

Department of Gastroenterology, Shanghai First People's Hospital, Shanghai Jiaotong University, Shanghai, China.

出版信息

J Dig Dis. 2008 May;9(2):63-7. doi: 10.1111/j.1751-2980.2008.00323.x.

Abstract

Insulin resistance is the basis of both non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MetS), the two conditions are often found in the same individual. The mortality of patients with NAFLD is significantly higher than that among the general population and cardiovascular risk may compete with liver-related risk in dictating the final outcome. Recent prospective studies have reported that NAFLD is associated with an increased incidence of MetS and type 2 diabetes mellitus, independent of obesity and other components of MetS. Thus, NAFLD may not only be a liver disease but also an early mediator of type 2 diabetes mellitus and MetS. The biological mechanisms by which NAFLD contributes to a higher risk of developing metabolic disorders are not fully understood. However, the fatty liver could contribute in the same way as visceral adipose tissue to insulin resistance, systemic inflammation and oxidative stress, while the decreased serum adiponectin concentrations might also be part of the mechanism. In contemporary clinical practice, it has become mandatory to evaluate the metabolic risk factors in NAFLD patients and to consider careful surveillance and aggressive treatment, not only of the resultant liver disease, but also of the possible underlying metabolic and vascular complications. Future studies might address the question whether earlier adjustment to a more efficient lifestyle or a pharmacological treatment that mobilizes fat out of the liver could reduce these risks.

摘要

胰岛素抵抗是非酒精性脂肪性肝病(NAFLD)和代谢综合征(MetS)的共同基础,这两种病症常出现在同一个体中。NAFLD患者的死亡率显著高于普通人群,在决定最终结局方面,心血管风险可能与肝脏相关风险相互竞争。最近的前瞻性研究报告称,NAFLD与MetS及2型糖尿病发病率增加相关,独立于肥胖和MetS的其他组分。因此,NAFLD可能不仅是一种肝脏疾病,还是2型糖尿病和MetS的早期介导因素。NAFLD导致代谢紊乱风险增加的生物学机制尚未完全明确。然而,脂肪肝可能与内脏脂肪组织一样,通过导致胰岛素抵抗、全身炎症和氧化应激来发挥作用,而血清脂联素浓度降低也可能是该机制的一部分。在当代临床实践中,评估NAFLD患者的代谢危险因素并考虑进行仔细监测和积极治疗已成为必要,这不仅是针对由此产生的肝脏疾病,还包括可能潜在的代谢和血管并发症。未来的研究可能会探讨早期调整为更有效的生活方式或采用促使脂肪从肝脏中移出的药物治疗是否能够降低这些风险。

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