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4M13产生的发酵美拉德反应产物改变2型糖尿病合并结肠炎小鼠的肠道微生物群并改善功能障碍

Fermented Maillard Reaction Products by 4M13 Alters the Intestinal Microbiota and Improves Dysfunction in Type 2 Diabetic Mice with Colitis.

作者信息

Jeong Yu-Jin, Park Ho-Young, Nam Han-Kyul, Lee Kwang-Won

机构信息

Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, 1, 5-ga, Anam-dong, Sungbuk-gu, Seoul 02841, Korea.

Research Division of Food Functionality, Korea Food Research Institute, Wanju 55365, Korea.

出版信息

Pharmaceuticals (Basel). 2021 Mar 28;14(4):299. doi: 10.3390/ph14040299.

DOI:10.3390/ph14040299
PMID:33800583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8066505/
Abstract

Inflammatory bowel disease is a chronic relapsing disease. Multiple factors can cause inflammatory bowel disease (IBD), including diet, imbalance of the immune system, and impaired intestinal barrier function. Type 2 diabetes mellitus is a complex and chronic metabolic disease caused by a combination of insulin resistance and an ineffective insulin secretory response. The co-occurrence of these two diseases, demonstrating interrelated effects within the gut microbiota, has been frequently reported. This study evaluated the effects of a fermented glycated conjugate of whey protein and galactose with 4M13 (FMRP) to prevent type 2 diabetes mellitus with inflammatory bowel disease. C57BLKS/J- db/db mice were orally administered FMRP for 14 consecutive days and 2% dextran sulfate sodium (DSS) in water ad libitum for 5 days to induce colitis. FMRP-fed mice showed improved insulin secretion and symptoms of colitis. Compared to the DSS group, the FMRP group showed a decreased abundance of six bacterial genera and increased abundance of and . In cecal contents, the levels of short-chain fatty acids increased in the FMRP group compared to those in the DSS group. Continuous administration of FMRP thus may improve the homeostasis of not only insulin secretion and inflammation, but also the intestinal environment in inflammatory bowel disease and type 2 diabetes mellitus.

摘要

炎症性肠病是一种慢性复发性疾病。多种因素可导致炎症性肠病(IBD),包括饮食、免疫系统失衡和肠道屏障功能受损。2型糖尿病是一种由胰岛素抵抗和无效胰岛素分泌反应共同引起的复杂慢性代谢疾病。这两种疾病的共同出现,在肠道微生物群中表现出相互关联的影响,已被频繁报道。本研究评估了乳清蛋白和半乳糖与4M13的发酵糖化共轭物(FMRP)预防2型糖尿病合并炎症性肠病的效果。将C57BLKS/J-db/db小鼠连续14天口服给予FMRP,并在水中自由饮用2%的硫酸葡聚糖钠(DSS)5天以诱导结肠炎。喂食FMRP的小鼠胰岛素分泌和结肠炎症状有所改善。与DSS组相比,FMRP组六个细菌属的丰度降低, 和 的丰度增加。在盲肠内容物中,FMRP组的短链脂肪酸水平比DSS组有所增加。因此,持续给予FMRP不仅可以改善胰岛素分泌和炎症的稳态,还可以改善炎症性肠病和2型糖尿病中的肠道环境。

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