Apigenin Ameliorates Insulin Resistance in 3T3-L1 Adipocytes: Establishment of a New Insulin Resistance Model Induced by Combined Treatments

文献类型： 外文期刊

第一作者： Guo, Xiaoxuan

作者： Guo, Xiaoxuan;Xia, Bing;Qian, Yongzhong;Qiu, Jing;Liu, Sha;Dong, Ying

作者机构：

关键词： adipocyte; apigenin; fructose; insulin resistance; palmitate acid; TNF-alpha

期刊名称：MOLECULAR NUTRITION & FOOD RESEARCH （ 影响因子：4.2； 五年影响因子：5.0 ）

ISSN： 1613-4125

年卷期： 2025 年 69 卷 5 期

页码：

收录情况： SCI

摘要： Adipose tissue dysfunction due to insulin resistance (IR) plays a central role in the development of metabolic diseases. Obesity-associated IR greatly attributes to low-grade inflammation and high circulating levels of FFAs and sugar. 3T3-L1 adipocytes exposed to a mixture of TNF-alpha, fructose, and palmitate acid for 24 h were validated as a model to simulate the pathogenesis of IR in obese people under a high-fat-fructose diet. Results show that the combined induction medium (CIM) successfully induced IR in 3T3-L1 adipocytes by impairing insulin signaling pathway. In the meantime, MAPK (JNK, ERK) pathway and NF kappa B p65 were activated, which are signs of inflammation response. Moreover, CIM caused mitochondrial dysfunction and oxidative stress. In addition, endoplasmic reticulum stress (ER stress) was evoked by CIM through activating IRE1 alpha/XBP1s, eIF2 alpha, and ATF6. Apigenin could efficiently relieve IR in adipocytes through sensitizing insulin signaling pathway, exerting antioxidant activity, blocking the NF kappa B pathway, and suppressing ER stress. The present study may provide new tools in discovering preventive and intervention strategies for IR caused by low-grade inflammation and high-fat-fructose diets and provide a basis for the application of apigenin in IR and other IR-related diseases.

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