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脂肪组织炎症是否会导致肥胖患者非酒精性脂肪性肝病的发生?

Does adipose tissue inflammation drive the development of non-alcoholic fatty liver disease in obesity?

机构信息

Department of Biomedicine, Unit of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal; NPqM - Núcleo de Pesquisa em Micronutrientes, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, Brasil.

Department of Biomedicine, Unit of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal; i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.

出版信息

Clin Res Hepatol Gastroenterol. 2020 Sep;44(4):394-402. doi: 10.1016/j.clinre.2019.10.001. Epub 2020 Feb 7.

DOI:10.1016/j.clinre.2019.10.001
PMID:32044284
Abstract

Obesity, an increasingly common problem in modern societies, is associated with acquired metabolic disturbances. In this perspective, the development of insulin resistance is now recognized to be initiated by inflammation of the adipose tissue, but the events that lead to this inflammation are still vague. Furthermore, visceral adipose tissue plays a significant role in obesity pathophysiology and in its clinical effects, such as non-alcoholic fatty liver disease (NAFLD). Among the possible mechanisms linking NAFLD and obesity, we focused on Visfatin/NAMPT, mostly produced by macrophages infiltrated in adipose tissue and a biomarker of the inflammatory cascade affecting hepatic inflammation in NAFLD. We also addressed the signalling pathway triggered by the binding of VEGF-B to its receptor, which mediates lipid fluxes throughout the body, being a promising target to prevent ectopic lipid accumulation. We reviewed the available literature on the topic and we suggest a crosstalk between adipose tissue inflammation and NAFLD in order to provide new insights about the putative mechanisms involved in the development of NAFLD in the obesity context. A better understanding of the pathophysiological processes underlying NAFLD will allow the development of new therapeutic approaches.

摘要

肥胖症是现代社会日益普遍的问题,与后天代谢紊乱有关。从这一角度来看,胰岛素抵抗的发展现在被认为是由脂肪组织的炎症引起的,但导致这种炎症的事件仍不清楚。此外,内脏脂肪组织在肥胖症的病理生理学及其临床影响(如非酒精性脂肪性肝病 (NAFLD))中发挥着重要作用。在可能将 NAFLD 和肥胖联系起来的机制中,我们重点关注 Visfatin/NAMPT,它主要由浸润脂肪组织的巨噬细胞产生,是影响 NAFLD 肝炎症的炎症级联反应的生物标志物。我们还研究了 VEGF-B 与其受体结合所触发的信号通路,该通路介导全身脂质通量,是预防异位脂质积累的有前途的靶点。我们回顾了该主题的现有文献,并提出了脂肪组织炎症和 NAFLD 之间的相互作用,以便提供有关肥胖症背景下 NAFLD 发展中涉及的潜在机制的新见解。对 NAFLD 潜在病理生理过程的更好理解将允许开发新的治疗方法。

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