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高糖饮食会导致微生物群组成发生变化,并增加小鼠对鼠伤寒沙门氏菌感染的易感性。

A high-sucrose diet causes microbiota composition shift and promotes the susceptibility of mice to Typhimurium infection.

作者信息

Liu Jiaxiu, Liu Huanhuan, Teng Yue, Qin Ningbo, Ren Xiaomeng, Xia Xiaodong

机构信息

Dalian Polytechnic University, China.

出版信息

Food Funct. 2023 Mar 20;14(6):2836-2846. doi: 10.1039/d2fo03467k.

Abstract

A westernized diet characterized by high fat and sugar is tightly associated with the development of metabolic diseases and inflammatory bowel disease. Although a high-fat diet has been extensively studied for its involvement in various diseases, fewer studies have examined the impact of a high-sugar diet on the development of certain diseases, particularly enteric infections. This study aimed to explore the effect of a high sucrose diet on Typhimurium-induced infection. C57BL/6 mice received a normal diet (Control) or a high sucrose diet (HSD) for eight weeks and then were infected by Typhimurium. The high-sugar diet profoundly altered the relative abundance of certain microbial taxa. and were more abundant in normal diet-fed mice than in HSD-fed mice. Moreover, short-chain fatty acids (SCFAs) and branched-chain fatty acids (BCFAs) were significantly higher in mice from the control group than the HSD group. More Typhimurium counts in feces and other tissues were observed in HSD-fed mice after infection. Tight junction proteins and antimicrobial peptides were significantly decreased in HSD-fed mice. Fecal microbiota transplantation (FMT) demonstrated that mice that received normal fecal microbiota had lower Typhimurium burdens compared with mice that received HSD fecal microbiota, indicating that the altered microbial communities are associated with the severity of infection. Together, these findings suggest that the excessive intake of sucrose disturbs intestinal homeostasis and predisposes mice to -induced infection.

摘要

以高脂肪和高糖为特征的西式饮食与代谢性疾病和炎症性肠病的发展密切相关。尽管高脂肪饮食因其与各种疾病的关联已得到广泛研究,但较少有研究考察高糖饮食对某些疾病,特别是肠道感染发展的影响。本研究旨在探讨高蔗糖饮食对鼠伤寒沙门氏菌诱导感染的影响。C57BL/6小鼠接受正常饮食(对照组)或高蔗糖饮食(HSD)八周,然后感染鼠伤寒沙门氏菌。高糖饮食深刻改变了某些微生物类群的相对丰度。在正常饮食喂养的小鼠中比在HSD喂养的小鼠中更为丰富。此外,对照组小鼠的短链脂肪酸(SCFAs)和支链脂肪酸(BCFAs)显著高于HSD组。感染后,在HSD喂养的小鼠粪便和其他组织中观察到更多的鼠伤寒沙门氏菌计数。HSD喂养的小鼠紧密连接蛋白和抗菌肽显著减少。粪便微生物群移植(FMT)表明,接受正常粪便微生物群的小鼠与接受HSD粪便微生物群的小鼠相比,鼠伤寒沙门氏菌负担更低,这表明改变的微生物群落与感染的严重程度相关。总之,这些发现表明,过量摄入蔗糖会扰乱肠道稳态,使小鼠易患鼠伤寒沙门氏菌诱导的感染。

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