Insulin resistance (IR) continues to pose a major threat to public health due to its role in the pathogenesis of metabolic syndrome and its ever-increasing prevalence on a global scale. The aim of the current study was to investigate the efficacy of Anxa2 in obesity-induced IR through the mediation of the NF-kappaB signaling pathway. Microanay analysis was performed to screen differentially expressed genes associated with obesity. To verify whether Anxa2 was differentially expressed in IR triggered by obesity, IR mouse models were established in connection with a high-fat diet (HFD). In the mouse IR model, the role of differentially expressed Anxa2 in glycometabolism and IR was subsequently detected. To investigate the effect of Anxa2 on IR and its correlation with inflammation, a palmitic acid (PA)-induced IR cell model was established, with the relationship between Anxa2 and the NF-kappaB signaling pathway investigated accordingly. Anxa2 was determined to be highly expressed in IR. Silencing Anxa2 was shown to inhibit IR triggered by obesity.
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机译：胰岛素抵抗 （IR） 继续对公众健康构成重大威胁，因为它在代谢综合征的发病机制中的作用及其在全球范围内的患病率不断增加。本研究的目的是通过介导 NF-κB 信号通路来研究 Anxa2 在肥胖诱导的 IR 中的疗效。进行显微分析以筛选与肥胖相关的差异表达基因。为了验证 Anxa2 是否在肥胖引发的 IR 中差异表达，建立了与高脂肪饮食 （HFD） 相关的 IR 小鼠模型。在小鼠 IR 模型中，随后检测差异表达的 Anxa2 在糖代谢和 IR 中的作用。为研究Anxa2对IR的影响及其与炎症的相关性，建立了棕榈酸（PA）诱导的IR细胞模型，并研究了Anxa2与NF-kappaB信号通路的关系。Anxa2 被确定在 IR 中高度表达。沉默 Anxa2 被证明可以抑制肥胖引发的 IR。
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