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脂肪组织炎症对胰岛素抵抗影响的最新进展。

Recent advances in the effect of adipose tissue inflammation on insulin resistance.

机构信息

The Second Clinical College of China Medical University, Shenyang, Liaoning 110122, China.

出版信息

Cell Signal. 2024 Aug;120:111229. doi: 10.1016/j.cellsig.2024.111229. Epub 2024 May 17.

Abstract

Obesity is one of the major risk factors for diabetes. Excessive accumulation of fat leads to inflammation of adipose tissue, which can increase the risk of developing diabetes. Obesity-related chronic inflammation can result in anomalies in glucose-lipid metabolism and insulin resistance, and it is a major cause of β-cell dysfunction in diabetes mellitus. Thus, a long-term tissue inflammatory response is crucial for metabolic diseases, particularly type 2 diabetes. Chronic inflammation associated with obesity increases oxidative stress, secretes inflammatory factors, modifies endocrine variables, and interferes with insulin signalling pathways, all of which contribute to insulin resistance and glucose tolerance. Insulin resistance and diabetes are ultimately caused by chronic inflammation in the stomach, pancreas, liver, muscle, and fat tissues. In this article, we systematically summarize the latest research progress on the mechanisms of adipose tissue inflammation and insulin resistance, as well as the mechanisms of cross-talk between adipose tissue inflammation and insulin resistance, with a view to providing some meaningful therapeutic strategies for the treatment of insulin resistance by controlling adipose tissue inflammation.

摘要

肥胖是糖尿病的主要危险因素之一。脂肪过度堆积会导致脂肪组织炎症,从而增加患糖尿病的风险。肥胖相关的慢性炎症可导致糖脂代谢和胰岛素抵抗异常,是糖尿病中β细胞功能障碍的主要原因。因此,长期的组织炎症反应对代谢性疾病,特别是 2 型糖尿病至关重要。与肥胖相关的慢性炎症会增加氧化应激,分泌炎症因子,改变内分泌变量,并干扰胰岛素信号通路,所有这些都会导致胰岛素抵抗和葡萄糖耐量受损。胰岛素抵抗和糖尿病最终是由胃、胰腺、肝脏、肌肉和脂肪组织的慢性炎症引起的。本文系统总结了脂肪组织炎症与胰岛素抵抗的机制以及脂肪组织炎症与胰岛素抵抗相互作用的机制的最新研究进展,以期为通过控制脂肪组织炎症治疗胰岛素抵抗提供一些有意义的治疗策略。

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