Zou Pei, Li Xueyan, Wang Liping, She Ying, Xiao Chenyang, Peng Yang, Qian Xu, Luo Peng, Wei Shaofeng
The Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of, Education, Guizhou Provincial Engineering Research Center of Ecological Food Innovation, Collaborative Innovation Center for Prevention and Control of Endemic and Ethnic Regional Diseases Co-constructed by the Province and Ministry, School of Public Health, Guizhou Medical University, Guiyang, 561113, China.
Department of Nutrition and Food Hygiene, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 210029, China.
Mol Nutr Food Res. 2024 Dec;68(24):e2400392. doi: 10.1002/mnfr.202400392. Epub 2024 Nov 26.
Grifola 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.
High-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.
These 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.
灰树花多糖（GFP）在调节2型糖尿病（T2DM）方面具有积极作用，但其调节机制的认识仍有限。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是否能通过调节肝脏炎症来调节T2DM及其潜在机制的问题尚未见报道。
采用高脂饮食（HFD）联合链脲佐菌素（STZ）注射的大鼠模型和脂多糖（LPS）处理的骨髓来源巨噬细胞（BMDM）模型。结果表明，GFP干预可减轻T2DM大鼠的体重减轻和高血糖症状，此外还可降低FINS、HOMA-IR、IPGTT-AUC和IPITT-AUC。同时，GFP干预可降低T2DM大鼠肝脏组织中炎症因子的分泌水平，增加抗炎因子的分泌水平。此外，GFP可减少肝脏组织中的巨噬细胞浸润，抑制巨噬细胞M1型极化，并促进M2型极化。
这些结果表明，GFP干预可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。这些发现为GFP在T2DM的早期预防和治疗中提供了新的证据。
