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Lactobacillus pentosus MJM60383 Inhibits Lipid Accumulation in Caenorhabditis elegans Induced by Enterobacter cloacae and Glucose
Gut microbiota are known to play an important role in obesity. Enterobacter cloacae, a Gram-negative bacterium, has been considered a pathogenic bacterium related to obesity in the gut. In this study, we established an obesity model of C. elegans by feeding E. cloacae combined with a high glucose di...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9820548/ https://www.ncbi.nlm.nih.gov/pubmed/36613723 http://dx.doi.org/10.3390/ijms24010280 |
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author | Gu, Mingkun Werlinger, Pia Cho, Joo-Hyung Jang, Nari Choi, Shin Sik Suh, Joo-Won Cheng, Jinhua |
author_facet | Gu, Mingkun Werlinger, Pia Cho, Joo-Hyung Jang, Nari Choi, Shin Sik Suh, Joo-Won Cheng, Jinhua |
author_sort | Gu, Mingkun |
collection | PubMed |
description | Gut microbiota are known to play an important role in obesity. Enterobacter cloacae, a Gram-negative bacterium, has been considered a pathogenic bacterium related to obesity in the gut. In this study, we established an obesity model of C. elegans by feeding E. cloacae combined with a high glucose diet (HGD), which significantly induced lipid accumulation. An anti-lipid mechanism study revealed that the fatty acid composition and the expression level of fat metabolism-related genes were altered by feeding E. cloacae to C. elegans under HGD conditions. Lactic acid bacteria that showed antagonistic activity against E. cloacae were used to screen anti-obesity candidates in this model. Among them, L. pentosus MJM60383 (MJM60383) showed good antagonistic activity. C. eleans fed with MJM60383 significantly reduced lipid accumulation and triglyceride content. The ratio of C18:1Δ9/C18:0 was also changed in C. elegans by feeding MJM60383. In addition, the expression level of genes related to fatty acid synthesis was significantly decreased and the genes related to fatty acid β-oxidation were up-regulated by feeding MJM60383. Moreover, MJM60383 also exhibited a high adhesive ability to Caco-2 cells and colonized the gut of C. elegans. Thus, L. pentosus MJM60383 can be a promising candidate for anti-obesity probiotics. To the best of our knowledge, this is the first report that uses E. cloacae combined with a high-glucose diet to study the interactions between individual pathogens and probiotics in C. elegans. |
format | Online Article Text |
id | pubmed-9820548 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-98205482023-01-07 Lactobacillus pentosus MJM60383 Inhibits Lipid Accumulation in Caenorhabditis elegans Induced by Enterobacter cloacae and Glucose Gu, Mingkun Werlinger, Pia Cho, Joo-Hyung Jang, Nari Choi, Shin Sik Suh, Joo-Won Cheng, Jinhua Int J Mol Sci Article Gut microbiota are known to play an important role in obesity. Enterobacter cloacae, a Gram-negative bacterium, has been considered a pathogenic bacterium related to obesity in the gut. In this study, we established an obesity model of C. elegans by feeding E. cloacae combined with a high glucose diet (HGD), which significantly induced lipid accumulation. An anti-lipid mechanism study revealed that the fatty acid composition and the expression level of fat metabolism-related genes were altered by feeding E. cloacae to C. elegans under HGD conditions. Lactic acid bacteria that showed antagonistic activity against E. cloacae were used to screen anti-obesity candidates in this model. Among them, L. pentosus MJM60383 (MJM60383) showed good antagonistic activity. C. eleans fed with MJM60383 significantly reduced lipid accumulation and triglyceride content. The ratio of C18:1Δ9/C18:0 was also changed in C. elegans by feeding MJM60383. In addition, the expression level of genes related to fatty acid synthesis was significantly decreased and the genes related to fatty acid β-oxidation were up-regulated by feeding MJM60383. Moreover, MJM60383 also exhibited a high adhesive ability to Caco-2 cells and colonized the gut of C. elegans. Thus, L. pentosus MJM60383 can be a promising candidate for anti-obesity probiotics. To the best of our knowledge, this is the first report that uses E. cloacae combined with a high-glucose diet to study the interactions between individual pathogens and probiotics in C. elegans. MDPI 2022-12-23 /pmc/articles/PMC9820548/ /pubmed/36613723 http://dx.doi.org/10.3390/ijms24010280 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Gu, Mingkun Werlinger, Pia Cho, Joo-Hyung Jang, Nari Choi, Shin Sik Suh, Joo-Won Cheng, Jinhua Lactobacillus pentosus MJM60383 Inhibits Lipid Accumulation in Caenorhabditis elegans Induced by Enterobacter cloacae and Glucose |
title | Lactobacillus pentosus MJM60383 Inhibits Lipid Accumulation in Caenorhabditis elegans Induced by Enterobacter cloacae and Glucose |
title_full | Lactobacillus pentosus MJM60383 Inhibits Lipid Accumulation in Caenorhabditis elegans Induced by Enterobacter cloacae and Glucose |
title_fullStr | Lactobacillus pentosus MJM60383 Inhibits Lipid Accumulation in Caenorhabditis elegans Induced by Enterobacter cloacae and Glucose |
title_full_unstemmed | Lactobacillus pentosus MJM60383 Inhibits Lipid Accumulation in Caenorhabditis elegans Induced by Enterobacter cloacae and Glucose |
title_short | Lactobacillus pentosus MJM60383 Inhibits Lipid Accumulation in Caenorhabditis elegans Induced by Enterobacter cloacae and Glucose |
title_sort | lactobacillus pentosus mjm60383 inhibits lipid accumulation in caenorhabditis elegans induced by enterobacter cloacae and glucose |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9820548/ https://www.ncbi.nlm.nih.gov/pubmed/36613723 http://dx.doi.org/10.3390/ijms24010280 |
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