دورية أكاديمية

An early-life microbiota metabolite protects against obesity by regulating intestinal lipid metabolism.

التفاصيل البيبلوغرافية
العنوان: An early-life microbiota metabolite protects against obesity by regulating intestinal lipid metabolism.
المؤلفون: Shelton CD; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA., Sing E; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA., Mo J; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA., Shealy NG; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA., Yoo W; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang 37673, Republic of Korea., Thomas J; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA., Fitz GN; Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA., Castro PR; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Laboratory of Immunoinflammation, Department of Genetics, Evolution, Microbiology, and Immunology, Institute of Biology, University of Campinas, Campinas, São Paulo 12083-862, Brazil., Hickman TT; Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA., Torres TP; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA., Foegeding NJ; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA., Zieba JK; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA., Calcutt MW; Mass Spectrometry Research Center and Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA., Codreanu SG; Center for Innovative Technology and Department of Chemistry, Vanderbilt University, Nashville, TN 37232, USA., Sherrod SD; Center for Innovative Technology and Department of Chemistry, Vanderbilt University, Nashville, TN 37232, USA., McLean JA; Center for Innovative Technology and Department of Chemistry, Vanderbilt University, Nashville, TN 37232, USA., Peck SH; Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA; Department of Biomedical Engineering, Vanderbilt University School of Engineering, Nashville, TN 37232, USA; Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA., Yang F; Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA; Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN 37232, USA., Markham NO; Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA; Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, TN, USA; Vanderbilt Institute of Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, TN 37232, USA., Liu M; Department of Pathology and Molecular Medicine, Metabolic Diseases Institute, University of Cincinnati College of Medicine, Cincinnati, OH 45237, USA., Byndloss MX; Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Institute of Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Digestive Disease Center, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Vanderbilt Microbiome Innovation Center, Vanderbilt University, Nashville, TN 37235, USA; Howard Hughes Medical Institute, Vanderbilt University Medical Center, Nashville, TN 37232, USA. Electronic address: mariana.x.byndloss@vumc.org.
المصدر: Cell host & microbe [Cell Host Microbe] 2023 Oct 11; Vol. 31 (10), pp. 1604-1619.e10. Date of Electronic Publication: 2023 Oct 03.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 101302316 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1934-6069 (Electronic) Linking ISSN: 19313128 NLM ISO Abbreviation: Cell Host Microbe Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Cambridge, Mass. : Cell Press
مواضيع طبية MeSH: Pediatric Obesity* , Microbiota*, Humans ; Child ; Animals ; Mice ; Lipid Metabolism ; Diet, High-Fat/adverse effects ; Anti-Bacterial Agents ; Polyesters ; Mice, Inbred C57BL
مستخلص: The mechanisms by which the early-life microbiota protects against environmental factors that promote childhood obesity remain largely unknown. Using a mouse model in which young mice are simultaneously exposed to antibiotics and a high-fat (HF) diet, we show that Lactobacillus species, predominant members of the small intestine (SI) microbiota, regulate intestinal epithelial cells (IECs) to limit diet-induced obesity during early life. A Lactobacillus-derived metabolite, phenyllactic acid (PLA), protects against metabolic dysfunction caused by early-life exposure to antibiotics and a HF diet by increasing the abundance of peroxisome proliferator-activated receptor γ (PPAR-γ) in SI IECs. Therefore, PLA is a microbiota-derived metabolite that activates protective pathways in the small intestinal epithelium to regulate intestinal lipid metabolism and prevent antibiotic-associated obesity during early life.
Competing Interests: Declaration of interests The authors declare no competing interests.
(Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)
التعليقات: Comment in: Cell Metab. 2023 Dec 5;35(12):2099-2100. (PMID: 38056427)
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معلومات مُعتمدة: IK2 BX005699 United States BX BLRD VA; T32 DK007673 United States DK NIDDK NIH HHS; S10 OD023475 United States OD NIH HHS; R01 DK131104 United States DK NIDDK NIH HHS; P30 DK058404 United States DK NIDDK NIH HHS; S10 OD021630 United States OD NIH HHS; T32 AI112541 United States AI NIAID NIH HHS; S10 OD026929 United States OD NIH HHS; P30 EY008126 United States EY NEI NIH HHS; T32 ES007028 United States ES NIEHS NIH HHS; R01 AI168302 United States AI NIAID NIH HHS; U24 DK059637 United States DK NIDDK NIH HHS; IK2 BX005401 United States BX BLRD VA; P30 DK020593 United States DK NIDDK NIH HHS; P30 CA068485 United States CA NCI NIH HHS; F31 AI161882 United States AI NIAID NIH HHS
فهرسة مساهمة: Keywords: Lactobacillus; antibiotics; arachnoid barrier; brain fibroblasts; early-life; intestinal epithelium; leptomeninges; metabolism; microbiota; obesity; single-cell RNA sequencing; tricellular junction
المشرفين على المادة: 0 (Anti-Bacterial Agents)
0 (Polyesters)
تواريخ الأحداث: Date Created: 20231005 Date Completed: 20231026 Latest Revision: 20240320
رمز التحديث: 20240321
مُعرف محوري في PubMed: PMC10593428
DOI: 10.1016/j.chom.2023.09.002
PMID: 37794592
قاعدة البيانات: MEDLINE
الوصف
تدمد:1934-6069
DOI:10.1016/j.chom.2023.09.002