肝脏因子:揭示肝脏组织与胰岛素抵抗和炎症之间的分子和细胞机制。

IF 3.1 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM Acta Diabetologica Pub Date : 2024-07-20 DOI:10.1007/s00592-024-02335-9
Xiaolei Miao, Arian Alidadipour, Vian Saed, Firooze Sayyadi, Yasaman Jadidi, Maryam Davoudi, Fatemeh Amraee, Nastaran Jadidi, Reza Afrisham
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摘要

非酒精性脂肪肝(NAFLD)引起的胰岛素抵抗是全球普遍存在的一种疾病,是个人饮食习惯和生活方式欠佳在社会中的一种表现。这种形式的胰岛素抵抗是导致 2 型糖尿病(T2DM)的关键因素。新的证据表明,肝脏分泌的激素类物质--肝动因在胰岛素抵抗的形成和 2 型糖尿病的最终发病中发挥着重要作用。肝脏因子对肝外代谢调节产生影响。它们的主要功能包括影响脂肪细胞、胰腺细胞、肌肉和大脑,从而通过向靶组织发出信号,在影响人体新陈代谢方面发挥关键作用。本综述探讨了最重要的肝脏激素,每种激素都有不同的影响。我们的综述显示,Fetuin-A 通过作为 Toll 样受体 4 (TLR-4) 的内源性配体,促进脂质诱导的胰岛素抵抗。FGF21 通过阻断脂肪细胞和脂肪组织中核因子-κB(NF-κB)的核转位来减轻糖尿病患者的炎症反应,同时还能改善葡萄糖代谢。ANGPTL6 可增强肌肉中的 AMPK 和胰岛素信号转导,抑制葡萄糖生成。Follistatin 可通过与 TGF-β 家族成员相互作用来影响胰岛素抵抗和炎症反应。阿托品与磷酸烯醇丙酮酸羧激酶 1(PCK1)呈正相关,PCK1 是葡萄糖生成的关键调节因子。本文将深入探讨肝脏激素对非酒精性脂肪肝、炎症和 T2DM 的影响,并特别关注胰岛素抵抗。目的是了解这些新近发现的激素对疾病发展的影响及其潜在的生理和病理机制。
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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Hepatokines: unveiling the molecular and cellular mechanisms connecting hepatic tissue to insulin resistance and inflammation

Insulin resistance arising from Non-Alcoholic Fatty Liver Disease (NAFLD) stands as a prevalent global ailment, a manifestation within societies stemming from individuals’ suboptimal dietary habits and lifestyles. This form of insulin resistance emerges as a pivotal factor in the development of type 2 diabetes mellitus (T2DM). Emerging evidence underscores the significant role of hepatokines, as hepatic-secreted hormone-like entities, in the genesis of insulin resistance and eventual onset of type 2 diabetes. Hepatokines exert influence over extrahepatic metabolism regulation. Their principal functions encompass impacting adipocytes, pancreatic cells, muscles, and the brain, thereby playing a crucial role in shaping body metabolism through signaling to target tissues. This review explores the most important hepatokines, each with distinct influences. Our review shows that Fetuin-A promotes lipid-induced insulin resistance by acting as an endogenous ligand for Toll-like receptor 4 (TLR-4). FGF21 reduces inflammation in diabetes by blocking the nuclear translocation of nuclear factor-κB (NF-κB) in adipocytes and adipose tissue, while also improving glucose metabolism. ANGPTL6 enhances AMPK and insulin signaling in muscle, and suppresses gluconeogenesis. Follistatin can influence insulin resistance and inflammation by interacting with members of the TGF-β family. Adropin show a positive correlation with phosphoenolpyruvate carboxykinase 1 (PCK1), a key regulator of gluconeogenesis. This article delves into hepatokines’ impact on NAFLD, inflammation, and T2DM, with a specific focus on insulin resistance. The aim is to comprehend the influence of these recently identified hormones on disease development and their underlying physiological and pathological mechanisms.

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来源期刊
Acta Diabetologica
Acta Diabetologica 医学-内分泌学与代谢
CiteScore
7.30
自引率
2.60%
发文量
180
审稿时长
2 months
期刊介绍: Acta Diabetologica is a journal that publishes reports of experimental and clinical research on diabetes mellitus and related metabolic diseases. Original contributions on biochemical, physiological, pathophysiological and clinical aspects of research on diabetes and metabolic diseases are welcome. Reports are published in the form of original articles, short communications and letters to the editor. Invited reviews and editorials are also published. A Methodology forum, which publishes contributions on methodological aspects of diabetes in vivo and in vitro, is also available. The Editor-in-chief will be pleased to consider articles describing new techniques (e.g., new transplantation methods, metabolic models), of innovative importance in the field of diabetes/metabolism. Finally, workshop reports are also welcome in Acta Diabetologica.
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