饮食中的胰岛素通过肠-胰腺轴改善肥胖引起的严重急性胰腺炎
Xin Li1, Pan Zheng1, Yaoyu Zou1
1Department of Gastroenterology, Jiangxi Provincial Key Laboratory of Digestive Diseases, Jiangxi Clinical Research Center for Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Gut microbes
|December 9, 2024
概括
食纤维的胰岛素通过调节肠道细菌和增加有益的短链脂肪酸 (SCFA) 来保护肥胖小鼠免受严重的胰腺炎的影响. 这突出了胰岛素中的胰岛素.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
背景情况:
- 肥胖会加剧急性胰腺炎 (AP) 的严重程度.
- 肠道微生物群的失生有助于AP的病变发生.
- 饮食干预对调节AP肠道微生物群的作用尚不清楚.
研究的目的:
- 为了研究胰岛素对高脂肪饮食 (HFD) 诱导的严重AP的影响.
- 探索肠道微生物群和短链脂肪酸 (SCFA) 在胰岛素保护作用中的作用.
- 阐明涉及基因素脱乙酶3 (HDAC3) 和巨细胞两极分化的潜在机制.
主要方法:
- 给HFD养小鼠的胰岛素.
- 使用无菌小鼠和便微生物群移植 (FMT) 来评估微生物群依赖性.
- 分析了肠道微生物群组成,便中的SCFA水平,肠道屏障完整性和帕内斯细胞功能.
- 研究了SCFA,HDAC3抑制和巨细胞极化作用.
主要成果:
- 在依赖肠道微生物群的HFD食小鼠中,胰腺损伤和全身炎症因胰岛素而减轻.
- 胰岛素改变了肠道微生物群,抑制了像Escherichia Shigella这样的病原体,并增加了Akkermansia.
- 胰岛素增加了SCFA,加强了肠道屏障,恢复了帕内斯细胞,这些效应取决于SCFA.
- 通过抑制HDAC3和调节巨细胞极化,SCFA,特别是丁酸盐,改善了胰腺和肠道损伤.
结论:
- 胰岛素通过肠道微生物群调节和SCFA产生,对与肥胖相关的严重AP产生保护作用.
- 通过抑制HDAC3而起作用的SCFA在改善胰腺和肠道损伤方面发挥着至关重要的作用.
- 针对肠道微生物群-胰腺轴,使用像胰岛素这样的益生菌,为严重的AP提供了潜在的治疗策略.
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