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首页> 外文期刊>Cell metabolism >Nonalcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases
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Nonalcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases

机译：非酒精性脂肪肝病作为代谢和肝病的Nexus

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摘要

NAFLD is closely linked with hepatic insulin resistance. Accumulation of hepatic diacylglycerol activates PKC-epsilon, impairing insulin receptor activation and insulin-stimulated glycogen synthesis. Peripheral insulin resistance indirectly influences hepatic glucose and lipid metabolism by increasing flux of substrates that promote lipogenesis (glucose and fatty acids) and gluconeogenesis (glycerol and fatty acid-derived acetyl-CoA, an allosteric activator of pyruvate carboxylase). Weight loss with diet or bariatric surgery effectively treats NAFLD, but drugs specifically approved for NAFLD are not available. Some new pharmacological strategies act broadly to alter energy balance or influence pathways that contribute to NAFLD (e.g., agonists for PPAR gamma, PPAR alpha/delta, FXR and analogs for FGF-21, and GLP-1). Others specifically inhibit key enzymes involved in lipid synthesis (e.g., mitochondrial pyruvate carrier, acetyl-CoA carboxylase, stearoyl-CoA desaturase, and monoacyl-and diacyl-glycerol transferases). Finally, a novel class of liver-targeted mitochondrial uncoupling agents increases hepatocellular energy expenditure, reversing the metabolic and hepatic complications of NAFLD.
机译：NAFLD与肝脏胰岛素抵抗密切相关。肝脏二酰甘油的积累激活PKCε，损害胰岛素受体激活和胰岛素刺激的糖原合成。外周胰岛素抵抗通过增加促进脂肪生成（葡萄糖和脂肪酸）和糖异生（甘油和脂肪酸衍生的乙酰辅酶A，丙酮酸羧化酶的变构激活剂）的底物流量间接影响肝脏葡萄糖和脂质代谢。通过节食或减肥手术减肥可以有效治疗NAFLD，但没有专门批准用于NAFLD的药物。一些新的药理学策略广泛作用于改变能量平衡或影响导致NAFLD的途径（例如PPARγ、PPARα/δ、FXR和FGF-21类似物以及GLP-1的激动剂）。其他酶则特别抑制参与脂质合成的关键酶（如线粒体丙酮酸载体、乙酰辅酶A羧化酶、硬脂酰辅酶A去饱和酶、单酰基和二酰基甘油转移酶）。最后，一类新的肝靶向线粒体解偶联剂增加肝细胞能量消耗，逆转NAFLD的代谢和肝脏并发症。

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