Cargando…

Pediococcus acidilactici CECT9879 (pA1c) Counteracts the Effect of a High-Glucose Exposure in C. elegans by Affecting the Insulin Signaling Pathway (IIS)

The increasing prevalence of metabolic syndrome-related diseases, including type-2 diabetes and obesity, makes it urgent to develop new alternative therapies, such as probiotics. In this study, we have used Caenorhabditis elegans under a high-glucose condition as a model to examine the potential pro...

Descripción completa

Detalles Bibliográficos
Autores principales: Yavorov-Dayliev, Deyan, Milagro, Fermín I., Ayo, Josune, Oneca, María, Aranaz, Paula
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8910957/
https://www.ncbi.nlm.nih.gov/pubmed/35269839
http://dx.doi.org/10.3390/ijms23052689
_version_ 1784666649331236864
author Yavorov-Dayliev, Deyan
Milagro, Fermín I.
Ayo, Josune
Oneca, María
Aranaz, Paula
author_facet Yavorov-Dayliev, Deyan
Milagro, Fermín I.
Ayo, Josune
Oneca, María
Aranaz, Paula
author_sort Yavorov-Dayliev, Deyan
collection PubMed
description The increasing prevalence of metabolic syndrome-related diseases, including type-2 diabetes and obesity, makes it urgent to develop new alternative therapies, such as probiotics. In this study, we have used Caenorhabditis elegans under a high-glucose condition as a model to examine the potential probiotic activities of Pediococcus acidilactici CECT9879 (pA1c). The supplementation with pA1c reduced C. elegans fat accumulation in a nematode growth medium (NGM) and in a high-glucose (10 mM) NGM medium. Moreover, treatment with pA1c counteracted the effect of the high glucose by reducing reactive oxygen species by 20%, retarding the aging process and extending the nematode median survival (>2 days in comparison with untreated control worms). Gene expression analyses demonstrated that the probiotic metabolic syndrome-alleviating activities were mediated by modulation of the insulin/IGF-1 signaling pathway (IIS) through the reversion of the glucose-nuclear-localization of daf-16 and the overexpression of ins-6 and daf-16 mediators, increased expression of fatty acid (FA) peroxisomal β-oxidation genes, and downregulation of FA biosynthesis key genes. Taken together, our data suggest that pA1c could be considered a potential probiotic strain for the prevention of the metabolic syndrome-related disturbances and highlight the use of C. elegans as an appropriate in vivo model for the study of the mechanisms underlying these diseases.
format Online
Article
Text
id pubmed-8910957
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-89109572022-03-11 Pediococcus acidilactici CECT9879 (pA1c) Counteracts the Effect of a High-Glucose Exposure in C. elegans by Affecting the Insulin Signaling Pathway (IIS) Yavorov-Dayliev, Deyan Milagro, Fermín I. Ayo, Josune Oneca, María Aranaz, Paula Int J Mol Sci Article The increasing prevalence of metabolic syndrome-related diseases, including type-2 diabetes and obesity, makes it urgent to develop new alternative therapies, such as probiotics. In this study, we have used Caenorhabditis elegans under a high-glucose condition as a model to examine the potential probiotic activities of Pediococcus acidilactici CECT9879 (pA1c). The supplementation with pA1c reduced C. elegans fat accumulation in a nematode growth medium (NGM) and in a high-glucose (10 mM) NGM medium. Moreover, treatment with pA1c counteracted the effect of the high glucose by reducing reactive oxygen species by 20%, retarding the aging process and extending the nematode median survival (>2 days in comparison with untreated control worms). Gene expression analyses demonstrated that the probiotic metabolic syndrome-alleviating activities were mediated by modulation of the insulin/IGF-1 signaling pathway (IIS) through the reversion of the glucose-nuclear-localization of daf-16 and the overexpression of ins-6 and daf-16 mediators, increased expression of fatty acid (FA) peroxisomal β-oxidation genes, and downregulation of FA biosynthesis key genes. Taken together, our data suggest that pA1c could be considered a potential probiotic strain for the prevention of the metabolic syndrome-related disturbances and highlight the use of C. elegans as an appropriate in vivo model for the study of the mechanisms underlying these diseases. MDPI 2022-02-28 /pmc/articles/PMC8910957/ /pubmed/35269839 http://dx.doi.org/10.3390/ijms23052689 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
Yavorov-Dayliev, Deyan
Milagro, Fermín I.
Ayo, Josune
Oneca, María
Aranaz, Paula
Pediococcus acidilactici CECT9879 (pA1c) Counteracts the Effect of a High-Glucose Exposure in C. elegans by Affecting the Insulin Signaling Pathway (IIS)
title Pediococcus acidilactici CECT9879 (pA1c) Counteracts the Effect of a High-Glucose Exposure in C. elegans by Affecting the Insulin Signaling Pathway (IIS)
title_full Pediococcus acidilactici CECT9879 (pA1c) Counteracts the Effect of a High-Glucose Exposure in C. elegans by Affecting the Insulin Signaling Pathway (IIS)
title_fullStr Pediococcus acidilactici CECT9879 (pA1c) Counteracts the Effect of a High-Glucose Exposure in C. elegans by Affecting the Insulin Signaling Pathway (IIS)
title_full_unstemmed Pediococcus acidilactici CECT9879 (pA1c) Counteracts the Effect of a High-Glucose Exposure in C. elegans by Affecting the Insulin Signaling Pathway (IIS)
title_short Pediococcus acidilactici CECT9879 (pA1c) Counteracts the Effect of a High-Glucose Exposure in C. elegans by Affecting the Insulin Signaling Pathway (IIS)
title_sort pediococcus acidilactici cect9879 (pa1c) counteracts the effect of a high-glucose exposure in c. elegans by affecting the insulin signaling pathway (iis)
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8910957/
https://www.ncbi.nlm.nih.gov/pubmed/35269839
http://dx.doi.org/10.3390/ijms23052689
work_keys_str_mv AT yavorovdaylievdeyan pediococcusacidilacticicect9879pa1ccounteractstheeffectofahighglucoseexposureincelegansbyaffectingtheinsulinsignalingpathwayiis
AT milagrofermini pediococcusacidilacticicect9879pa1ccounteractstheeffectofahighglucoseexposureincelegansbyaffectingtheinsulinsignalingpathwayiis
AT ayojosune pediococcusacidilacticicect9879pa1ccounteractstheeffectofahighglucoseexposureincelegansbyaffectingtheinsulinsignalingpathwayiis
AT onecamaria pediococcusacidilacticicect9879pa1ccounteractstheeffectofahighglucoseexposureincelegansbyaffectingtheinsulinsignalingpathwayiis
AT aranazpaula pediococcusacidilacticicect9879pa1ccounteractstheeffectofahighglucoseexposureincelegansbyaffectingtheinsulinsignalingpathwayiis