Altered lipid metabolism and the development of metabolic-associated fatty liver disease.

IF 3.8 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Current opinion in lipidology Pub Date : 2024-08-01 Epub Date: 2024-03-14 DOI:10.1097/MOL.0000000000000933
Christy Foster, Charles A Gagnon, Ambika P Ashraf
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Abstract

Purpose of review: An increasing amount of research has underscored the significant role of lipoproteins in the pathogenesis of metabolic-associated fatty liver disease (MAFLD). This comprehensive review examines the intricate relationship between lipoprotein abnormalities and the development of MAFLD.

Recent findings: Atherogenic dyslipidemia seen in insulin resistance states play a significant role in initiating and exacerbating hepatic lipid accumulation. There are also specific genetic factors ( PNPLA3 , TM6SF2 , MBOAT7 , HSD17B13 , GCKR- P446L) and transcription factors (SREBP-2, FXR, and LXR9) that increase susceptibility to both lipoprotein disorders and MAFLD. Most monogenic primary lipid disorders do not cause hepatic steatosis unless accompanied by metabolic stress. Hepatic steatosis occurs in the presence of secondary systemic metabolic stress in conjunction with predisposing environmental factors that lead to insulin resistance. Identifying specific aberrant lipoprotein metabolic factors promoting hepatic fat accumulation and subsequently exacerbating steatohepatitis will shed light on potential targets for therapeutic interventions.

Summary: The clinical implications of interconnection between genetic factors and an insulin resistant environment that predisposes MAFLD is many fold. Potential therapeutic strategies in preventing or mitigating MAFLD progression include lifestyle modifications, pharmacological interventions, and emerging therapies targeting aberrant lipoprotein metabolism.

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脂质代谢改变与代谢相关性脂肪肝的发展。
综述的目的:越来越多的研究强调了脂蛋白在代谢相关性脂肪肝(MAFLD)发病机制中的重要作用。这篇综合性综述探讨了脂蛋白异常与代谢相关性脂肪肝发病之间错综复杂的关系:最新发现:胰岛素抵抗状态下的致动脉粥样硬化性血脂异常在启动和加剧肝脏脂质积累方面起着重要作用。还有一些特定的遗传因素(PNPLA3、TM6SF2、MBOAT7、HSD17B13、GCKR-P446L)和转录因子(SREBP-2、FXR 和 LXR9)会增加脂蛋白紊乱和 MAFLD 的易感性。大多数单基因原发性脂质紊乱不会导致肝脂肪变性,除非伴有代谢压力。肝脂肪变性会在继发性全身代谢应激和导致胰岛素抵抗的易感环境因素共同作用下发生。总结:遗传因素和胰岛素抵抗环境之间的相互联系易导致肝脂肪肝,其临床意义是多方面的。预防或缓解 MAFLD 进展的潜在治疗策略包括改变生活方式、药物干预和针对异常脂蛋白代谢的新兴疗法。
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来源期刊
Current opinion in lipidology
Current opinion in lipidology 医学-内分泌学与代谢
CiteScore
6.70
自引率
4.50%
发文量
64
审稿时长
6-12 weeks
期刊介绍: With its easy-to-digest reviews on important advances in world literature, Current Opinion in Lipidology offers expert evaluation on a wide range of topics from six key disciplines including nutrition and metabolism, genetics and molecular biology, and hyperlipidaemia and cardiovascular disease. Published bimonthly, each issue covers in detail the most pertinent advances in these fields from the previous year. This is supplemented by a section of Bimonthly Updates, which deliver an insight into new developments at the cutting edge of the disciplines covered in the journal.
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