Non alcoholic fatty liver disease: pathogenesis, role of (TNF-α, IL-6) in hepatic inflammation and future potential nutraceutical treatment

Safaa A. Faheem, Noha M Saeed, R. N. El-Naga, S. Azab
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引用次数: 1

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a pathological condition characterized by the accumulation of triglycerides (TGs) in the hepatocytes and has usually been associated with hyperlipidemia, obesity, and insulin resistance. Besides, it is a progressive condition that has become one of the most common liver disorder in developed countries and is usually accompanied by increased cardiovascular and land liver disease mortality. NAFLD is a spectrum of liver disorders, progressing from simple steatosis to non-alcoholic steatohepatitis which is characterized by inflammation and hepatocellular injury then fibrosis which finally results in cirrhosis and even hepatocellular cancer. However, the molecular mechanism contributing to NAFLD progression is not fully understood. Its pathogenesis has usually been recognized by the "double-insult" hypothesis. the "first insult" includes accumulation of TGs in the hepatocyte, followed by a "second insult" where inflammatory mediators convince hepatocellular injury, inflammation, and fibrosis. In NAFLD, insulin resistance initiates the hepatic steatosis by different mechanisms. Furthermore, it was shown that NAFLD is associated with an inhibition of fatty acid oxidation in the mitochondria and an increase in the release of very-low-density lipoproteins. This review discusses the pathophysiology of NAFLD and the role of insulin resistance, obesity and inflammatory markers in the initiation of NAFLD. in addition to the different Therapeutic approaches for NAFLD.
非酒精性脂肪性肝病:发病机制,(TNF-α, IL-6)在肝脏炎症中的作用和未来潜在的营养治疗
非酒精性脂肪性肝病(NAFLD)是一种以肝细胞中甘油三酯(tg)积累为特征的病理状况,通常与高脂血症、肥胖和胰岛素抵抗有关。此外,它是一种进行性疾病,已成为发达国家最常见的肝脏疾病之一,通常伴有心血管和陆地肝病死亡率增加。NAFLD是一系列肝脏疾病,从单纯脂肪变性发展到非酒精性脂肪性肝炎,其特征是炎症和肝细胞损伤,然后纤维化,最终导致肝硬化甚至肝细胞癌。然而,促进NAFLD进展的分子机制尚不完全清楚。其发病机制通常被认为是“双重侮辱”假说。“第一次损伤”包括肝细胞中tg的积累,随后是“第二次损伤”,炎症介质导致肝细胞损伤、炎症和纤维化。在NAFLD中,胰岛素抵抗通过不同的机制引发肝脏脂肪变性。此外,研究表明NAFLD与线粒体中脂肪酸氧化的抑制和极低密度脂蛋白释放的增加有关。本文综述了NAFLD的病理生理学以及胰岛素抵抗、肥胖和炎症标志物在NAFLD发病中的作用。除了NAFLD不同的治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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