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来自决明子胶的甘露寡糖可改善糖尿病大鼠的炎症和葡萄糖代谢。

Manno-oligosaccharides from cassia seed gum ameliorate inflammation and improve glucose metabolism in diabetic rats.

机构信息

Key Laboratory of Food Bioengineering (China National Light Industry), College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.

Department of Nutrition and Health, College of Engineering, China Agricultural University, Beijing 100083, China.

出版信息

Food Funct. 2022 Jun 20;13(12):6674-6687. doi: 10.1039/d1fo03057d.

DOI:10.1039/d1fo03057d
PMID:35647651
Abstract

Functional oligosaccharides show anti-diabetic effects through inflammation regulation with improved glucose metabolism. In this study, novel prebiotics of manno-oligosaccharides from cassia seed gum (CMOS) were incorporated into the diet of streptozotocin (STZ) plus high-fat and high-sugar diet (HFSD)-induced rats. After feeding for 8 weeks, CMOS (300-1200 mg per kg b.w. per d) significantly ameliorated the fasting blood glucose level (7.1-8.2 mmol L) as compared with that of the model group (14.2 mmol L), where the area under the oral glucose tolerance test curve was decreased by 20.0%-24.5%. Meanwhile, CMOS prevented STZ plus HFSD-induced damage to islet tissue with a clear and integrated morphology and reduced the glucagon/insulin area ratio (by 97.9% for 300 mg per kg b.w. per d CMOS). CMOS also reduced metabolic endotoxemia and maintained intestinal integrity with recovered mRNA expression of and to the normal comparable level. Upon 16S rDNA sequencing, it was found that CMOS regulated the microbiota composition in the cecum with an increased relative abundance of , while that of was decreased. The molecular mechanisms involved in the anti-diabetic effects of CMOS were further studied. CMOS reduced the mRNA expression of and in the intestines of STZ plus HFSD-induced rats. Meanwhile, associated inflammasome activation in the intestine and liver with glucose metabolism disorder was inhibited by CMOS, resulting in reduced interleukin-1β secretion (by 38.8-46.4% for CMOS of 300-1200 mg per kg b.w. per d) and inflammation. Furthermore, CMOS regulated the AKT/IRS/AMPK signaling pathway and improved glucose metabolism in the liver. Findings obtained here implicated that CMOS could modulate metabolic-inflammation as a functional dietary supplement.

摘要

功能性低聚糖通过调节炎症改善葡萄糖代谢,从而发挥抗糖尿病作用。本研究将新型来源于决明子胶的甘露寡糖(CMOS)作为膳食补充剂添加到链脲佐菌素(STZ)加高脂高糖饮食(HFSD)诱导的大鼠饮食中。8 周喂养后,与模型组(14.2mmol/L)相比,CMOS(300-1200mg/kg bw/d)可显著改善空腹血糖水平(7.1-8.2mmol/L),口服葡萄糖耐量试验曲线下面积降低 20.0%-24.5%。同时,CMOS 可防止 STZ 加 HFSD 诱导的胰岛组织损伤,使胰岛形态清晰完整,降低胰高血糖素/胰岛素面积比(300mg/kg bw/d CMOS 降低 97.9%)。CMOS 还可降低代谢性内毒素血症,维持肠道完整性,恢复 和 的 mRNA 表达至正常可比水平。16S rDNA 测序发现,CMOS 可调节盲肠中的微生物组成,增加相对丰度较高的 ,同时降低 的相对丰度。进一步研究了 CMOS 抗糖尿病作用的分子机制。CMOS 可降低 STZ 加 HFSD 诱导大鼠肠道中 和 的 mRNA 表达。同时,CMOS 抑制肠和肝中与葡萄糖代谢紊乱相关的 相关炎性小体激活,导致白细胞介素-1β分泌减少(300-1200mg/kg bw/d CMOS 减少 38.8-46.4%)和炎症减轻。此外,CMOS 可调节 AKT/IRS/AMPK 信号通路,改善肝脏葡萄糖代谢。这些发现表明,CMOS 可以作为一种功能性膳食补充剂调节代谢-炎症。

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