ScopeGrifola frondosa polysaccharide (GFP) has a positive effect in regulating type 2 diabetes mellitus (T2DM), but the understanding of its regulatory mechanism is still limited. Accumulating evidence suggests that hepatic inflammation is crucial in the onset and progression of insulin resistance (IR) and T2DM. However, the question of whether GFP can modulate T2DM via regulating hepatic inflammation and the underlying mechanism has not yet been reported.Methods and resultsHigh‐fat diet (HFD) fed combined with streptozocin (STZ) injections rat model and Lipopolysaccharides (LPS)‐treated bone marrow‐derived macrophages (BMDM) model are used. The results showed that GFP intervention reduces weight loss and hyperglycemia symptoms, besides lowers FINS, HOMA‐IR, IPGTT‐AUC, and IPITT‐AUC in T2DM rats. Meanwhile, GFP intervention reduces the secretion level of inflammatory factors and increases the secretion level of anti‐inflammatory factors in the liver tissue of T2DM rats. Furthermore, GFP reduces macrophage infiltration in liver tissue, inhibits macrophage M1‐type polarization, and promotes M2‐type polarization.ConclusionsThese results suggest that GFP intervention could attenuate the hepatic inflammatory and insulin resistance in T2DM rats by inhibiting hepatic macrophage infiltration and modulating M1/M2 polarization. The findings provide new evidence for GFP in the early prevention and treatment of T2DM.

中文翻译：

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灰树多糖通过调节 2 型糖尿病大鼠肝脏巨噬细胞极化改善炎症


ScopeGrifola frondosa 多糖 （GFP） 对调节 2 型糖尿病 （T2DM） 具有积极作用，但对其调节机制的认识仍然有限。越来越多的证据表明，肝脏炎症在胰岛素抵抗 （IR） 和 T2DM 的发生和发展中至关重要。然而，GFP 是否可以通过调节肝脏炎症来调节 T2DM 及其潜在机制的问题尚未报道。方法和结果使用高脂饮食 （HFD） 喂养联合链脲佐菌素 （STZ） 注射大鼠模型和脂多糖 （LPS） 处理的骨髓衍生巨噬细胞 （BMDM） 模型。结果显示，GFP 干预可减轻体重减轻和高血糖症状，此外还降低了 T2DM 大鼠的 FINS 、 HOMA-IR 、 IPGTT-AUC 和 IPITT-AUC。同时，GFP 干预降低了 T2DM 大鼠肝组织中炎症因子的分泌水平，增加了抗炎因子的分泌水平。此外，GFP 减少肝组织中巨噬细胞的浸润，抑制巨噬细胞 M1 型极化，并促进 M2 型极化。结论这些结果表明，GFP 干预可以通过抑制肝脏巨噬细胞浸润和调节 M1/M2 极化来减轻 T2DM 大鼠的肝脏炎症和胰岛素抵抗。研究结果为 GFP 在 T2DM 的早期预防和治疗提供了新的证据。