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Effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in C57BL/6 mice
[PURPOSE]: The aim of this study was to investigate the effects of aerobic exercise training on a high fat diet (HFD)-induced fatty liver and its metabolic complications in C57BL/6 mice. [METHODS]: Mice at 5-month old (n = 30) were randomly assigned to standard chow (SC + CON, n = 10) and high-fat d...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Korean Society for Exercise Nutrition
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322024/ https://www.ncbi.nlm.nih.gov/pubmed/25671200 http://dx.doi.org/10.5717/jenb.2014.18.4.339 |
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author | Cho, Jinkyung Lee, Inhwan Kim, Donghyun Koh, Yeojung Kong, Jiyoung Lee, Sanghee Kang, Hyunsik |
author_facet | Cho, Jinkyung Lee, Inhwan Kim, Donghyun Koh, Yeojung Kong, Jiyoung Lee, Sanghee Kang, Hyunsik |
author_sort | Cho, Jinkyung |
collection | PubMed |
description | [PURPOSE]: The aim of this study was to investigate the effects of aerobic exercise training on a high fat diet (HFD)-induced fatty liver and its metabolic complications in C57BL/6 mice. [METHODS]: Mice at 5-month old (n = 30) were randomly assigned to standard chow (SC + CON, n = 10) and high-fat diet (HFD, n = 20), and they were subjected to SC and HFD, respectively, for 23-week. After 15-week of HFD, mice in the HFD group were further assigned to HFD (HFD + CON, n = 10) or exercise training (HFD + EX, n = 10) groups. The HFD + EX mice were subjected to aerobic treadmill running during the last 8-week of the 23-week HFD course. Outcomes included hepatic steatosis, insulin resistance, and expression of genes involved in mitochondrial function and/or fatty oxidation as well as de novo lipogenesis and/or triacylglycerol (TAG) synthesis. [RESULTS]: Treadmill running ameliorated impaired glucose tolerance and insulin resistance secondary to the HFD. The beneficial effects of treadmill running were associated with enhanced molecular markers of mitochondrial function and/or fatty acids oxidation (i.e., PPARα and CPT1a mRNAs, pAMPK/AMPK, pACC, and SIRT1 protein) as well as suppressed expression of de novo lipogenesis and/or TAG synthesis (i.e., SREBP1c, lipin1 and FAS mRNAs) in the liver. [CONCLUSION]: The current findings suggest that aerobic exercise training is an effective and non-pharmacological means to combat fatty liver and its metabolic complications in HFD-induced obese mice. |
format | Online Article Text |
id | pubmed-4322024 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Korean Society for Exercise Nutrition |
record_format | MEDLINE/PubMed |
spelling | pubmed-43220242015-02-10 Effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in C57BL/6 mice Cho, Jinkyung Lee, Inhwan Kim, Donghyun Koh, Yeojung Kong, Jiyoung Lee, Sanghee Kang, Hyunsik J Exerc Nutrition Biochem Original Paper [PURPOSE]: The aim of this study was to investigate the effects of aerobic exercise training on a high fat diet (HFD)-induced fatty liver and its metabolic complications in C57BL/6 mice. [METHODS]: Mice at 5-month old (n = 30) were randomly assigned to standard chow (SC + CON, n = 10) and high-fat diet (HFD, n = 20), and they were subjected to SC and HFD, respectively, for 23-week. After 15-week of HFD, mice in the HFD group were further assigned to HFD (HFD + CON, n = 10) or exercise training (HFD + EX, n = 10) groups. The HFD + EX mice were subjected to aerobic treadmill running during the last 8-week of the 23-week HFD course. Outcomes included hepatic steatosis, insulin resistance, and expression of genes involved in mitochondrial function and/or fatty oxidation as well as de novo lipogenesis and/or triacylglycerol (TAG) synthesis. [RESULTS]: Treadmill running ameliorated impaired glucose tolerance and insulin resistance secondary to the HFD. The beneficial effects of treadmill running were associated with enhanced molecular markers of mitochondrial function and/or fatty acids oxidation (i.e., PPARα and CPT1a mRNAs, pAMPK/AMPK, pACC, and SIRT1 protein) as well as suppressed expression of de novo lipogenesis and/or TAG synthesis (i.e., SREBP1c, lipin1 and FAS mRNAs) in the liver. [CONCLUSION]: The current findings suggest that aerobic exercise training is an effective and non-pharmacological means to combat fatty liver and its metabolic complications in HFD-induced obese mice. Korean Society for Exercise Nutrition 2014-12 2014-12-04 /pmc/articles/PMC4322024/ /pubmed/25671200 http://dx.doi.org/10.5717/jenb.2014.18.4.339 Text en ⓒ2014 The Korean Society for Exercise Nutrition This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Paper Cho, Jinkyung Lee, Inhwan Kim, Donghyun Koh, Yeojung Kong, Jiyoung Lee, Sanghee Kang, Hyunsik Effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in C57BL/6 mice |
title | Effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in C57BL/6 mice |
title_full | Effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in C57BL/6 mice |
title_fullStr | Effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in C57BL/6 mice |
title_full_unstemmed | Effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in C57BL/6 mice |
title_short | Effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in C57BL/6 mice |
title_sort | effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in c57bl/6 mice |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322024/ https://www.ncbi.nlm.nih.gov/pubmed/25671200 http://dx.doi.org/10.5717/jenb.2014.18.4.339 |
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