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不同剂量的蔗糖摄入对 DSS 诱导的结肠炎小鼠肠道微生物群和 PPAR-γ/MAPK/NF-κB 通路的影响不同。

Different Dose of Sucrose Consumption Divergently Influences Gut Microbiota and PPAR-γ/MAPK/NF-κB Pathway in DSS-Induced Colitis Mice.

机构信息

Tianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, China.

College of Food Science and Technology, Hebei Agricultural University, Baoding 071000, China.

出版信息

Nutrients. 2022 Jul 4;14(13):2765. doi: 10.3390/nu14132765.

Abstract

Sugar reduction and sugar control are advocated and gaining popularity around the world. Sucrose, as the widely consumed ingredient in our daily diet, has been reported a relation to gastrointestinal diseases. However, the role of sucrose in inflammatory bowel disease remains controversial. Hence, our study aimed to elucidate the potential role of three doses of sucrose on DSS-induced colitis in C57BL/6 mice and the underlying mechanisms. The results showed that low-dose sucrose intervention alleviated colitis in mice, reducing the expression of inflammatory cytokines and repairing mucosal damages. In contrast, high-dose sucrose intervention exacerbated colitis. Furthermore, three doses of sucrose administration markedly altered gut microbiota composition. Notably, the low-dose sucrose restored microbial dysfunction and enhanced the production of short chain fatty acids (SCFAs). Specifically, the abundance of SCFAs-producing bacteria , and were increased significantly in the LOW group. Consistently, PPAR-γ, activated by SCFAs, was elevated in the LOW group, thereby inhibiting the MAPK/NF-κB pathway. Together, our study demonstrates the differential effects of sucrose on colitis at different doses, providing a scientific basis for measuring and modifying the safe intake level of sugar and providing favorable evidence for implementing sugar reduction policies.

摘要

减少和控制糖的摄入在全球范围内得到了广泛的提倡和关注。蔗糖作为我们日常饮食中广泛消费的成分之一,与胃肠道疾病有关。然而,蔗糖在炎症性肠病中的作用仍存在争议。因此,我们的研究旨在阐明蔗糖的三个剂量对 C57BL/6 小鼠 DSS 诱导结肠炎的潜在作用及其潜在机制。结果表明,低剂量蔗糖干预减轻了小鼠的结肠炎,降低了炎症细胞因子的表达并修复了黏膜损伤。相比之下,高剂量蔗糖干预则加重了结肠炎。此外,蔗糖的三个剂量给药显著改变了肠道微生物群落的组成。值得注意的是,低剂量蔗糖恢复了微生物功能障碍并增强了短链脂肪酸(SCFA)的产生。具体而言,低剂量蔗糖组中产生 SCFA 的细菌 、 和 的丰度显著增加。一致地,SCFA 激活的 PPAR-γ 在低剂量蔗糖组中升高,从而抑制 MAPK/NF-κB 通路。总之,我们的研究表明蔗糖在不同剂量下对结肠炎的影响存在差异,为测量和调整糖的安全摄入量提供了科学依据,并为实施减糖政策提供了有利的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e65/9268685/d09257253272/nutrients-14-02765-g001.jpg

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