- Book学术

发布求助

文献互助智能选刊最新文献

IF 6 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver International Pub Date : 2025-03-07 DOI:10.1111/liv.70047

Hannele Yki-Järvinen, Panu K. Luukkonen

{"title":"Function of PNPLA3 I148M—Lessons From In Vivo Studies in Humans","authors":"Hannele Yki-Järvinen, Panu K. Luukkonen","doi":"10.1111/liv.70047","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Background and Aims</h3>\n \n <p>Steatotic liver disease (SLD) associated with insulin resistance (IR) and the metabolic syndrome (‘IR-SLD’) increases the risk of liver disease, type 2 diabetes and cardiovascular disease (CVD). SLD associated with the PNPLA3 I148M variant (‘PNPLA3-SLD’) also predisposes individuals to liver disease but protects against type 2 diabetes and CVD. Although in real life the two causes of SLD commonly co-exist, the opposite effects of ‘IR-SLD’ and ‘PNPLA3-SLD’ on CVD and liver disease suggest their pathogenesis differs.</p>\n </section>\n \n <section>\n \n <h3> Methods and Results</h3>\n \n <p>This review summarises human data comparing the effects of ‘IR-SLD’ and ‘PNPLA3-SLD’ on the human liver lipidome, hepatic handling of fatty acids, pathways of intrahepatocellular triglyceride synthesis, circulating lipids and lipoproteins and adipose tissue inflammation. We also discuss how steatosis in PNPLA3 I148M carriers leads to defects in mitochondrial function.</p>\n </section>\n </div>","PeriodicalId":18101,"journal":{"name":"Liver International","volume":"45 4","pages":""},"PeriodicalIF":6.0000,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/liv.70047","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Liver International","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/liv.70047","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}

引用次数: 0

摘要

背景和目的与胰岛素抵抗（IR）和代谢综合征（"IR-SLD"）相关的脂肪性肝病（SLD）会增加罹患肝病、2型糖尿病和心血管疾病（CVD）的风险。与 PNPLA3 I148M 变体相关的 SLD（"PNPLA3-SLD"）也易导致肝病，但可预防 2 型糖尿病和心血管疾病。尽管在现实生活中这两种 SLD 病因通常同时存在，但 "IR-SLD "和 "PNPLA3-SLD "对心血管疾病和肝病的影响截然相反，这表明它们的发病机制不同。方法和结果本综述总结了人类数据，比较了 "IR-SLD "和 "PNPLA3-SLD "对人类肝脏脂质组、肝脏处理脂肪酸、肝细胞内甘油三酯合成途径、循环脂质和脂蛋白以及脂肪组织炎症的影响。我们还讨论了 PNPLA3 I148M 携带者的脂肪变性如何导致线粒体功能缺陷。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Function of PNPLA3 I148M—Lessons From In Vivo Studies in Humans

查看原文本刊更多论文

Function of PNPLA3 I148M—Lessons From In Vivo Studies in Humans

Background and Aims

Steatotic liver disease (SLD) associated with insulin resistance (IR) and the metabolic syndrome (‘IR-SLD’) increases the risk of liver disease, type 2 diabetes and cardiovascular disease (CVD). SLD associated with the PNPLA3 I148M variant (‘PNPLA3-SLD’) also predisposes individuals to liver disease but protects against type 2 diabetes and CVD. Although in real life the two causes of SLD commonly co-exist, the opposite effects of ‘IR-SLD’ and ‘PNPLA3-SLD’ on CVD and liver disease suggest their pathogenesis differs.

Methods and Results

This review summarises human data comparing the effects of ‘IR-SLD’ and ‘PNPLA3-SLD’ on the human liver lipidome, hepatic handling of fatty acids, pathways of intrahepatocellular triglyceride synthesis, circulating lipids and lipoproteins and adipose tissue inflammation. We also discuss how steatosis in PNPLA3 I148M carriers leads to defects in mitochondrial function.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊

Liver International 医学-胃肠肝病学

CiteScore

13.90

自引率

4.50%

发文量

348

审稿时长

2 months

期刊介绍： Liver International promotes all aspects of the science of hepatology from basic research to applied clinical studies. Providing an international forum for the publication of high-quality original research in hepatology, it is an essential resource for everyone working on normal and abnormal structure and function in the liver and its constituent cells, including clinicians and basic scientists involved in the multi-disciplinary field of hepatology. The journal welcomes articles from all fields of hepatology, which may be published as original articles, brief definitive reports, reviews, mini-reviews, images in hepatology and letters to the Editor.