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肥胖中的胰岛素抵抗:基本改变概述

Insulin resistance in obesity: an overview of fundamental alterations.

作者信息

Barazzoni Rocco, Gortan Cappellari Gianluca, Ragni Maurizio, Nisoli Enzo

机构信息

Department of Medical, Surgical and Health Sciences, University of Trieste, Strada di Fiume, 447, 34149, Trieste, Italy.

Azienda Sanitaria Universitaria Integrata di Trieste (ASUITS), Trieste, Italy.

出版信息

Eat Weight Disord. 2018 Apr;23(2):149-157. doi: 10.1007/s40519-018-0481-6. Epub 2018 Feb 3.

DOI:10.1007/s40519-018-0481-6
PMID:29397563
Abstract

Obesity is a major health risk factor, and obesity-induced morbidity and complications account for huge costs for affected individuals, families, healthcare systems, and society at large. In particular, obesity is strongly associated with the development of insulin resistance, which in turn plays a key role in the pathogenesis of obesity-associated cardiometabolic complications, including metabolic syndrome components, type 2 diabetes, and cardiovascular diseases. Insulin sensitive tissues, including adipose tissue, skeletal muscle, and liver, are profoundly affected by obesity both at biomolecular and functional levels. Altered adipose organ function may play a fundamental pathogenetic role once fat accumulation has ensued. Modulation of insulin sensitivity appears to be, at least in part, related to changes in redox balance and oxidative stress as well as inflammation, with a relevant underlying role for mitochondrial dysfunction that may exacerbate these alterations. Nutrients and substrates as well as systems involved in host-nutrient interactions, including gut microbiota, have been also identified as modulators of metabolic pathways controlling insulin action. This review aims at providing an overview of these concepts and their potential inter-relationships in the development of insulin resistance, with particular regard to changes in adipose organ and skeletal muscle.

摘要

肥胖是一个主要的健康风险因素,肥胖引发的发病率和并发症给受影响的个人、家庭、医疗保健系统以及整个社会带来了巨大的成本。特别是,肥胖与胰岛素抵抗的发展密切相关,而胰岛素抵抗又在肥胖相关的心脏代谢并发症(包括代谢综合征成分、2型糖尿病和心血管疾病)的发病机制中起关键作用。胰岛素敏感组织,包括脂肪组织、骨骼肌和肝脏,在生物分子和功能水平上都受到肥胖的深刻影响。一旦出现脂肪堆积,脂肪器官功能的改变可能起着根本性的致病作用。胰岛素敏感性的调节似乎至少部分与氧化还原平衡和氧化应激以及炎症的变化有关,线粒体功能障碍在其中起着相关的潜在作用,可能会加剧这些改变。营养物质和底物以及参与宿主-营养相互作用的系统,包括肠道微生物群,也已被确定为控制胰岛素作用的代谢途径的调节因子。本综述旨在概述这些概念及其在胰岛素抵抗发展中的潜在相互关系,特别关注脂肪器官和骨骼肌的变化。

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Mitochondrial dysfunction in obesity.肥胖中的线粒体功能障碍。
Life Sci. 2018 Jan 1;192:26-32. doi: 10.1016/j.lfs.2017.11.019. Epub 2017 Nov 16.
2
Acylated ghrelin treatment normalizes skeletal muscle mitochondrial oxidative capacity and AKT phosphorylation in rat chronic heart failure.酰化 ghrelin 治疗可使慢性心力衰竭大鼠骨骼肌线粒体氧化能力和 AKT 磷酸化正常化。
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Amino acid supplements and metabolic health: a potential interplay between intestinal microbiota and systems control.
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Curr Nutr Rep. 2025 Jul 8;14(1):92. doi: 10.1007/s13668-025-00682-9.
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Association of SNPs in carbohydrate metabolism genes with insulin resistance indicators in the Mexican population.墨西哥人群中碳水化合物代谢基因单核苷酸多态性与胰岛素抵抗指标的关联
Nutr Metab (Lond). 2025 Jul 1;22(1):65. doi: 10.1186/s12986-025-00926-z.
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HF01 postbiotics reprogram gut microbial tryptophan metabolism to coordinate enterohepatic barrier-insulin signaling axis.HF01后生元可重新编程肠道微生物色氨酸代谢,以协调肠肝屏障-胰岛素信号轴。
Curr Res Food Sci. 2025 Jun 10;11:101111. doi: 10.1016/j.crfs.2025.101111. eCollection 2025.
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The role of cardiovascular disease in the association between estimated glucose disposal rate and chronic kidney disease.心血管疾病在估计的葡萄糖处置率与慢性肾脏病关联中的作用。
Sci Rep. 2025 May 8;15(1):16034. doi: 10.1038/s41598-025-00359-x.
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Insulin Resistance in Pediatric Obesity: From Mechanisms to Treatment Strategies.儿童肥胖中的胰岛素抵抗:从机制到治疗策略
Pediatr Diabetes. 2024 Jun 28;2024:2298306. doi: 10.1155/2024/2298306. eCollection 2024.
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Medicine (Baltimore). 2025 Apr 18;104(16):e42172. doi: 10.1097/MD.0000000000042172.
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Memantine abrogates testicular dysfunction induced by risperidone in rats with a potential role of ERK1/2-Nrf2-caspase-3 signaling pathway.美金刚可消除利培酮诱导的大鼠睾丸功能障碍,ERK1/2-Nrf2-半胱天冬酶-3信号通路可能发挥作用。
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Thyroid hormones induce browning of white fat.甲状腺激素诱导白色脂肪棕色化。
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