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菊粉通过重塑肠道菌群调节2型糖尿病小鼠的肠胶质细胞功能来抑制炎症反应。

Inulin Inhibits the Inflammatory Response through Modulating Enteric Glial Cell Function in Type 2 Diabetic Mellitus Mice by Reshaping Intestinal Flora.

作者信息

Li Meng-Ying, Duan Jia-Qi, Wang Xiao-Hui, Liu Meng, Yang Qiao-Yi, Li Yan, Cheng Kun, Liu Han-Qiang, Wang Feng

机构信息

The Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, The Shaanxi Provincial Key Laboratory of Environmental Health Hazard Assessment and Protection, The Shaanxi Provincial Key Laboratory of Free Radical Biology and Medicine, Department of Health Education and Management, School of Preventive Medicine, Air Force Medical University, West Changle Road No. 169, Xi'an, Shaanxi 710032, China.

Department of Endocrinology, Xijing Hospital, Air Force Medical University, West Changle Road No. 127, Xi'an, Shaanxi 710032, China.

出版信息

ACS Omega. 2023 Sep 28;8(40):36729-36743. doi: 10.1021/acsomega.3c03055. eCollection 2023 Oct 10.

DOI:10.1021/acsomega.3c03055
PMID:37841129
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10568710/
Abstract

Inulin, a commonly used dietary fiber supplement, is capable of modulating the gut microbiome. Chronic inflammation resulting from metabolic abnormalities and gut flora dysfunction plays a significant role in the development of type 2 diabetes mellitus (T2DM). Our research has demonstrated that inulin administration effectively reduced colonic inflammation in T2DM mice by inducing changes in the gut microbiota and increasing the concentration of butyric acid, which in turn modulated the function of enteric glial cells (EGCs). Experiments conducted on T2DM mice revealed that inulin administration led to an increase in the / ratio and the concentration of butyric acid in the colon. The anti-inflammatory effects of altered gastrointestinal flora and its metabolites were further confirmed through fecal microbiota transplantation. Butyric acid was found to inhibit the activation of the κB inhibitor kinase β/nuclear factor κB pathway, regulate the expression levels of interleukin-6 and tumor necrosis factor-α, suppress the abnormal activation of EGCs, and prevent the release of inflammatory factors by EGCs. Similar results were observed in vitro experiments with butyric acid. Our findings demonstrate that inulin, by influencing the intestinal flora, modifies the activity of EGCs to effectively reduce colonic inflammation in T2DM mice.

摘要

菊粉是一种常用的膳食纤维补充剂,能够调节肠道微生物群。由代谢异常和肠道菌群功能障碍引起的慢性炎症在2型糖尿病(T2DM)的发生发展中起重要作用。我们的研究表明,给予菊粉可通过诱导肠道微生物群的变化和增加丁酸浓度来有效减轻T2DM小鼠的结肠炎症,进而调节肠胶质细胞(EGC)的功能。对T2DM小鼠进行的实验表明,给予菊粉可导致结肠中/比值和丁酸浓度增加。通过粪便微生物群移植进一步证实了改变的胃肠道菌群及其代谢产物的抗炎作用。发现丁酸可抑制κB抑制激酶β/核因子κB途径的激活,调节白细胞介素-6和肿瘤坏死因子-α的表达水平,抑制EGC的异常激活,并阻止EGC释放炎症因子。在丁酸的体外实验中也观察到了类似结果。我们的研究结果表明,菊粉通过影响肠道菌群,改变EGC的活性,有效减轻T2DM小鼠的结肠炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/de12ff22262b/ao3c03055_0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/0f1285b80f9c/ao3c03055_0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/c0e7a648cd27/ao3c03055_0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/2230c813a92e/ao3c03055_0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/93d48056a958/ao3c03055_0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/8646207be55f/ao3c03055_0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/de12ff22262b/ao3c03055_0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/0f1285b80f9c/ao3c03055_0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/c0e7a648cd27/ao3c03055_0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/2230c813a92e/ao3c03055_0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/93d48056a958/ao3c03055_0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/8646207be55f/ao3c03055_0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5573/10568710/de12ff22262b/ao3c03055_0006.jpg

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A diet enriched in omega-3 PUFA and inulin prevents type 1 diabetes by restoring gut barrier integrity and immune homeostasis in NOD mice.富含 ω-3PUFA 和菊粉的饮食可通过恢复 NOD 小鼠的肠道屏障完整性和免疫稳态来预防 1 型糖尿病。
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Clinical Evidence and Proposed Mechanisms for Cardiovascular and Kidney Benefits from Sodium-Glucose Co-transporter-2 Inhibitors.
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