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Nutrients, Physical Activity, and Mitochondrial Dysfunction in the Setting of Metabolic Syndrome
Metabolic syndrome (MetS) is a cluster of metabolic risk factors for diabetes, coronary heart disease, non-alcoholic fatty liver disease, and some tumors. It includes insulin resistance, visceral adiposity, hypertension, and dyslipidemia. MetS is primarily linked to lipotoxicity, with ectopic fat de...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10004804/ https://www.ncbi.nlm.nih.gov/pubmed/36904216 http://dx.doi.org/10.3390/nu15051217 |
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author | Lemos, Gabriela de Oliveira Torrinhas, Raquel Susana Waitzberg, Dan Linetzky |
author_facet | Lemos, Gabriela de Oliveira Torrinhas, Raquel Susana Waitzberg, Dan Linetzky |
author_sort | Lemos, Gabriela de Oliveira |
collection | PubMed |
description | Metabolic syndrome (MetS) is a cluster of metabolic risk factors for diabetes, coronary heart disease, non-alcoholic fatty liver disease, and some tumors. It includes insulin resistance, visceral adiposity, hypertension, and dyslipidemia. MetS is primarily linked to lipotoxicity, with ectopic fat deposition from fat storage exhaustion, more than obesity per se. Excessive intake of long-chain saturated fatty acid and sugar closely relates to lipotoxicity and MetS through several pathways, including toll-like receptor 4 activation, peroxisome proliferator-activated receptor-gamma regulation (PPARγ), sphingolipids remodeling, and protein kinase C activation. These mechanisms prompt mitochondrial dysfunction, which plays a key role in disrupting the metabolism of fatty acids and proteins and in developing insulin resistance. By contrast, the intake of monounsaturated, polyunsaturated, and medium-chain saturated (low-dose) fatty acids, as well as plant-based proteins and whey protein, favors an improvement in sphingolipid composition and metabolic profile. Along with dietary modification, regular exercises including aerobic, resistance, or combined training can target sphingolipid metabolism and improve mitochondrial function and MetS components. This review aimed to summarize the main dietary and biochemical aspects related to the physiopathology of MetS and its implications for mitochondrial machinery while discussing the potential role of diet and exercise in counteracting this complex clustering of metabolic dysfunctions. |
format | Online Article Text |
id | pubmed-10004804 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-100048042023-03-11 Nutrients, Physical Activity, and Mitochondrial Dysfunction in the Setting of Metabolic Syndrome Lemos, Gabriela de Oliveira Torrinhas, Raquel Susana Waitzberg, Dan Linetzky Nutrients Review Metabolic syndrome (MetS) is a cluster of metabolic risk factors for diabetes, coronary heart disease, non-alcoholic fatty liver disease, and some tumors. It includes insulin resistance, visceral adiposity, hypertension, and dyslipidemia. MetS is primarily linked to lipotoxicity, with ectopic fat deposition from fat storage exhaustion, more than obesity per se. Excessive intake of long-chain saturated fatty acid and sugar closely relates to lipotoxicity and MetS through several pathways, including toll-like receptor 4 activation, peroxisome proliferator-activated receptor-gamma regulation (PPARγ), sphingolipids remodeling, and protein kinase C activation. These mechanisms prompt mitochondrial dysfunction, which plays a key role in disrupting the metabolism of fatty acids and proteins and in developing insulin resistance. By contrast, the intake of monounsaturated, polyunsaturated, and medium-chain saturated (low-dose) fatty acids, as well as plant-based proteins and whey protein, favors an improvement in sphingolipid composition and metabolic profile. Along with dietary modification, regular exercises including aerobic, resistance, or combined training can target sphingolipid metabolism and improve mitochondrial function and MetS components. This review aimed to summarize the main dietary and biochemical aspects related to the physiopathology of MetS and its implications for mitochondrial machinery while discussing the potential role of diet and exercise in counteracting this complex clustering of metabolic dysfunctions. MDPI 2023-02-28 /pmc/articles/PMC10004804/ /pubmed/36904216 http://dx.doi.org/10.3390/nu15051217 Text en © 2023 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 | Review Lemos, Gabriela de Oliveira Torrinhas, Raquel Susana Waitzberg, Dan Linetzky Nutrients, Physical Activity, and Mitochondrial Dysfunction in the Setting of Metabolic Syndrome |
title | Nutrients, Physical Activity, and Mitochondrial Dysfunction in the Setting of Metabolic Syndrome |
title_full | Nutrients, Physical Activity, and Mitochondrial Dysfunction in the Setting of Metabolic Syndrome |
title_fullStr | Nutrients, Physical Activity, and Mitochondrial Dysfunction in the Setting of Metabolic Syndrome |
title_full_unstemmed | Nutrients, Physical Activity, and Mitochondrial Dysfunction in the Setting of Metabolic Syndrome |
title_short | Nutrients, Physical Activity, and Mitochondrial Dysfunction in the Setting of Metabolic Syndrome |
title_sort | nutrients, physical activity, and mitochondrial dysfunction in the setting of metabolic syndrome |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10004804/ https://www.ncbi.nlm.nih.gov/pubmed/36904216 http://dx.doi.org/10.3390/nu15051217 |
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