<br>脂肪酸转运蛋白 4 在代谢组织中的作用：对肥胖和脂肪肝疾病的见解。,Bioscience Reports

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脂肪酸转运蛋白 4 在代谢组织中的作用：对肥胖和脂肪肝疾病的见解。
Bioscience Reports ( IF 3.8 ) Pub Date : 2022-05-18 , DOI: 10.1042/bsr20211854
Huili Li _{1,

2} , Thomas Herrmann ₃ , Jessica Seeßle ₁ , Gerhard Liebisch ₄ , Uta Merle ₁ , Wolfgang Stremmel ₁ , Walee Chamulitrat ₁

Affiliation

脂肪酸（FA）代谢是提供结构物质、信号分子和能量的一系列过程。充足的证据表明，FA 摄取是由质膜转运蛋白介导的，包括 FA 转运蛋白 (FATP)、caveolin-1、脂肪酸转位酶 (FAT)/CD36 和脂肪酸结合蛋白。与其他 FA 转运蛋白不同，FATP 的功能一直存在争议，因为它们同时包含 FA 转运基序和脂酰辅酶 A 合成酶 (ACS)。广泛分布的 FATP4 不是直接的 FA 转运蛋白，但作为 ACS 发挥着主要功能。 FATP4 缺乏会导致小鼠和人类出现鱼鳞病早产综合征，该综合征与极性脂质抑制有关，但中性脂质（包括甘油三酯 (TG)）增加有关。这种转变在肠细胞、肝细胞和脂肪细胞特异性 Fatp4 缺陷小鼠中得到了广泛的表征。不同饮食诱导的肥胖和非肥胖脂肪肝下的突变体持续表现出血液非酯化游离脂肪酸和甘油的增加，表明TG的脂肪分解。本综述还重点关注 FATP4 在调节网络中的作用以及调节代谢组织（包括肠道、肝脏、肌肉和脂肪组织）中 FATP4 表达的因素。本文讨论了不同细胞类型中由于 FATP4 缺乏而引起的代谢紊乱，特别是与血脂有关的代谢紊乱。我们的结果可能不仅适用于 FATP4 突变的患者，而且还代表了脂质稳态失调的模型，从而为肥胖和脂肪肝疾病的发展提供了机制见解。

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Role of fatty acid transport protein 4 in metabolic tissues: insights into obesity and fatty liver disease.

Fatty acid (FA) metabolism is a series of processes that provide structural substances, signalling molecules and energy. Ample evidence has shown that FA uptake is mediated by plasma membrane transporters including FA transport proteins (FATPs), caveolin-1, fatty-acid translocase (FAT)/CD36, and fatty-acid binding proteins. Unlike other FA transporters, the functions of FATPs have been controversial because they contain both motifs of FA transport and fatty acyl-CoA synthetase (ACS). The widely distributed FATP4 is not a direct FA transporter but plays a predominant function as an ACS. FATP4 deficiency causes ichthyosis premature syndrome in mice and humans associated with suppression of polar lipids but an increase in neutral lipids including triglycerides (TGs). Such a shift has been extensively characterized in enterocyte-, hepatocyte-, and adipocyte-specific Fatp4-deficient mice. The mutants under obese and non-obese fatty livers induced by different diets persistently show an increase in blood non-esterified free fatty acids and glycerol indicating the lipolysis of TGs. This review also focuses on FATP4 role on regulatory networks and factors that modulate FATP4 expression in metabolic tissues including intestine, liver, muscle, and adipose tissues. Metabolic disorders especially regarding blood lipids by FATP4 deficiency in different cell types are herein discussed. Our results may be applicable to not only patients with FATP4 mutations but also represent a model of dysregulated lipid homeostasis, thus providing mechanistic insights into obesity and development of fatty liver disease.

更新日期：2022-05-18

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