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在高脂肪饮食诱导的肥胖小鼠中改善GLP-1分泌,从而调节葡萄糖恒温
Jie Liu1,2, Dandan Zhang1, Zihui Yang1
1National Center of Technology Innovation for Grain Industry (Comprehensive Utilization of Edible Byproducts), Beijing Technology & Business University, Beijing 100048, China.
Journal of agricultural and food chemistry
|October 19, 2023
概括
小麦基素 (ARs) 通过增强类似葡萄糖1 (GLP-1) 的分泌来改善葡萄糖平衡和胰岛素耐药性. ARs保护肠道内膜,促进有益的细菌,为肥胖提供饮食策略.
科学领域:
- 代谢学 代谢学 代谢学
- 肠道微生物组研究研究
- 营养生物化学 营养生物化学
背景情况:
- 小麦基复合素 (ARs) 在控制肥胖和胰岛素抵抗方面表现出潜力.
- 通过ARs影响葡萄糖类1 (GLP-1) 分泌的精确机制在很大程度上仍未被阐明.
- 了解AR对肠道健康和激素调节的影响对于代谢疾病管理至关重要.
研究的目的:
- 在高脂肪饮食 (HFD) 鼠标模型中研究ARs对GLP-1分泌和葡萄糖平衡的影响.
- 阐明潜在的机制,包括肠道屏障完整性,亡,线粒体功能和肠道微生物群调节.
- 用棕酸诱导的细胞模型在体外验证这些发现.
主要方法:
- 给C57BL/6J小鼠吃低脂肪饮食 (LFD),高脂肪饮食 (HFD) 或补充AR的高脂肪饮食9周.
- 用TUNEL染色,免疫光和传输电子显微镜来评估肠道屏障的完整性.
- 试验室研究涉及用棕酸 (PA) 和ARs治疗STC-1细胞,随后进行亡和线粒体功能分析.
- 分析了肠道微生物群组成和短链脂肪酸 (SCFA) 水平.
主要成果:
- ARs的干预显著改善了葡萄糖平衡,并在HFD小鼠中恢复了GLP-1水平.
- 治疗ARs缓解了HFD诱导的叶上皮损伤,减少了亡,并改善了线粒体功能.
- 在体外,AR增强了STC-1细胞中的GLP-1分泌,减少了细胞亡,并减轻了线粒体功能障碍.
- 抗药物增加了SCFA产生细菌 (例如,Bacteroides,Bifidobacterium,Akkermansia) 和SCFA水平,上调FFAR3和GLP-1R的表达.
结论:
- 小麦基醇可增强GLP-1分泌并改善葡萄糖平衡,可能通过肠道屏障保护和微生物群调节.
- ARs减轻棕酸诱导的细胞损伤和线粒体功能障碍,支持它们在代谢健康中的作用.
- 增加SCFA生产和随后的受体激活似乎是推动ARs对GLP-1分泌的有益作用的关键机制.
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