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牙周炎与肝脏和肠道炎症及血糖控制的相关性,以及SMFM2016-RK生物转化的影响。

Correlation of periodontitis with hepatic and intestinal inflammation and glycemic control, and effects of bioconverted by SMFM2016-RK.

作者信息

Lee Yewon, Yoon Yohan, Choi Kyoung-Hee

机构信息

Risk Analysis Research Center, Sookmyung Women's University, Seoul, Korea.

Department of Food and Nutrition, Sookmyung Women's University, Seoul, Korea.

出版信息

J Oral Microbiol. 2025 Mar 14;17(1):2473246. doi: 10.1080/20002297.2025.2473246. eCollection 2025.

DOI:10.1080/20002297.2025.2473246
PMID:40099142
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11912291/
Abstract

Periodontitis has been linked to systemic inflammation, however research on its role in causing systemic diseases remains limited. Recent studies explore probiotics for microbiome modulation and enhancing natural compound bioavailability. This study investigated periodontitis-related systemic disease mechanisms, and evaluated the mitigation effects of bioconversion product using SMFM2016-RK and extracts. Four types of bioconverted milk [BM1 ( SMFM2016-RK), BM2 (BM1 +  ethanol extract), BM3 (BM1 +  hot-water extract), and BM4 (BM1+ both extracts)] were studied in a periodontitis-induced rat model. Rats were divided into six groups: normal control, skim milk with ligature, and four BM groups with ligature.   Periodontitis induction elevated trabecular resorption (0.325 ± 0.057 mm³) and histopathological symptoms. Serum ALT (55.6 ± 6.6 U/L), glucose (261.7 ± 64.3 mg/dL), insulin (1.90 ± 0.87 ng/mL), inflammation in the liver and colon, and gluconeogenesis-related enzyme expression increased. Periodontitis-induced rats showed gut dysbiosis, with decreased level and increased level. BM3 administration significantly reduced the serum glucose (190.9 ± 27.8 mg/dL), ALT (40.5 ± 5.0 U/L), inflammation, and gluconeogenesis-related enzymes, while increasing tight junction proteins expression and phylum Actinobacteria levels in the gut microbiome. The findings highlight the systemic impact of periodontitis on inflammation, glycemic control, and gut microbiome balance. BM3 effectively alleviated these effects suggesting therapeutic potential.

摘要

牙周炎与全身炎症有关,然而关于其在引发全身性疾病中作用的研究仍然有限。最近的研究探索了用于调节微生物群和提高天然化合物生物利用度的益生菌。本研究调查了牙周炎相关的全身性疾病机制,并评估了使用SMFM2016 - RK和提取物的生物转化产物的缓解效果。在牙周炎诱导的大鼠模型中研究了四种类型的生物转化牛奶[BM1(SMFM2016 - RK)、BM2(BM1 +乙醇提取物)、BM3(BM1 +热水提取物)和BM4(BM1 +两种提取物)]。大鼠被分为六组:正常对照组、结扎脱脂牛奶组以及四个结扎的BM组。牙周炎诱导增加了小梁吸收(0.325±0.057mm³)和组织病理学症状。血清谷丙转氨酶(ALT)(55.6±6.6U/L)、葡萄糖(261.7±64.3mg/dL)、胰岛素(1.90±0.87ng/mL)、肝脏和结肠中的炎症以及糖异生相关酶表达增加。牙周炎诱导的大鼠表现出肠道菌群失调,水平降低而水平升高。给予BM3显著降低了血清葡萄糖(190.9±27.8mg/dL)、ALT(40.5±5.0U/L)、炎症和糖异生相关酶,同时增加了肠道微生物群中紧密连接蛋白的表达和放线菌门水平。这些发现突出了牙周炎对炎症、血糖控制和肠道微生物群平衡的全身性影响。BM3有效缓解了这些影响,表明其具有治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/2601b8c1eb6f/ZJOM_A_2473246_F0007_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/25f18b97f758/ZJOM_A_2473246_F0001_OC.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/3743d8684a5c/ZJOM_A_2473246_F0005a_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/a28179dd6899/ZJOM_A_2473246_F0005b_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/50b636d97b42/ZJOM_A_2473246_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/2601b8c1eb6f/ZJOM_A_2473246_F0007_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/25f18b97f758/ZJOM_A_2473246_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/cc94b69c80a1/ZJOM_A_2473246_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/9a5fc21b628a/ZJOM_A_2473246_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/d095274975f2/ZJOM_A_2473246_F0004a_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/cf56f46c38ea/ZJOM_A_2473246_F0004b_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/3743d8684a5c/ZJOM_A_2473246_F0005a_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/a28179dd6899/ZJOM_A_2473246_F0005b_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/50b636d97b42/ZJOM_A_2473246_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5470/11912291/2601b8c1eb6f/ZJOM_A_2473246_F0007_B.jpg

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本文引用的文献

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Microorganisms. 2024 Jun 25;12(7):1290. doi: 10.3390/microorganisms12071290.
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Spore-forming properties and enhanced oxygen tolerance of butyrate-producing Anaerostipes spp.产丁酸厌氧梭菌的孢子形成特性和耐氧能力增强
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Periodontitis may induce gut microbiota dysbiosis via salivary microbiota.
牙周炎可能通过唾液微生物群引起肠道微生物群失调。
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Identification of mucin degraders of the human gut microbiota.鉴定人类肠道微生物群中的粘蛋白降解物。
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Dysbiosis and Implication of the Gut Microbiota in Diabetic Retinopathy.肠道微生物群失调及其在糖尿病视网膜病变中的意义
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Periodontol 2000. 2020 Jun;83(1):7-13. doi: 10.1111/prd.12344.
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Mechanisms underlying the association between periodontitis and atherosclerotic disease.牙周炎与动脉粥样硬化性疾病相关性的潜在机制。
Periodontol 2000. 2020 Jun;83(1):90-106. doi: 10.1111/prd.12304.
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Aggregatibacter, A Low Abundance Pathobiont That Influences Biogeography, Microbial Dysbiosis, and Host Defense Capabilities in Periodontitis: The History of A Bug, And Localization of Disease.聚集杆菌,一种影响牙周炎生物地理学、微生物失调和宿主防御能力的低丰度致病共生菌:一种细菌的历史以及疾病的定位
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Regulation of host-microbe interactions at oral mucosal barriers by type 17 immunity.17 型免疫调节口腔黏膜屏障的宿主-微生物相互作用。
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