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Systemic regulation of L-carnitine in nutritional metabolism in zebrafish, Danio rerio
Excess fat accumulation has been observed widely in farmed fish; therefore, efficient lipid-lowering factors have obtained high attention in the current fish nutrition studies. Dietary L-carnitine can increase fatty acid β-oxidation in mammals, but has produced contradictory results in different fis...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5244368/ https://www.ncbi.nlm.nih.gov/pubmed/28102299 http://dx.doi.org/10.1038/srep40815 |
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author | Li, Jia-Min Li, Ling-Yu Qin, Xun Ning, Li-Jun Lu, Dong-Liang Li, Dong-Liang Zhang, Mei-Ling Wang, Xin Du, Zhen-Yu |
author_facet | Li, Jia-Min Li, Ling-Yu Qin, Xun Ning, Li-Jun Lu, Dong-Liang Li, Dong-Liang Zhang, Mei-Ling Wang, Xin Du, Zhen-Yu |
author_sort | Li, Jia-Min |
collection | PubMed |
description | Excess fat accumulation has been observed widely in farmed fish; therefore, efficient lipid-lowering factors have obtained high attention in the current fish nutrition studies. Dietary L-carnitine can increase fatty acid β-oxidation in mammals, but has produced contradictory results in different fish species. To date, the mechanisms of metabolic regulation of L-carnitine in fish have not been fully determined. The present study used zebrafish to investigate the systemic regulation of nutrient metabolism by dietary L-carnitine supplementation. L-carnitine significantly decreased the lipid content in liver and muscle, accompanied by increased concentrations of total and free carnitine in tissues. Meanwhile, L-carnitine enhanced mitochondrial β-oxidation activities and the expression of carnitine palmitoyltransferase 1 mRNA significantly, whereas it depressed the mRNA expression of adipogenesis-related genes. In addition, L-carnitine caused higher glycogen deposition in the fasting state, and increased and decreased the mRNA expressions of gluconeogenesis-related and glycolysis-related genes, respectively. L-carnitine also increased the hepatic expression of mTOR in the feeding state. Taken together, dietary L-carnitine supplementation decreased lipid deposition by increasing mitochondrial fatty acid β-oxidation, and is likely to promote protein synthesis. However, the L-carnitine-enhanced lipid catabolism would cause a decrease in glucose utilization. Therefore, L-carnitine has comprehensive effects on nutrient metabolism in fish. |
format | Online Article Text |
id | pubmed-5244368 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-52443682017-01-23 Systemic regulation of L-carnitine in nutritional metabolism in zebrafish, Danio rerio Li, Jia-Min Li, Ling-Yu Qin, Xun Ning, Li-Jun Lu, Dong-Liang Li, Dong-Liang Zhang, Mei-Ling Wang, Xin Du, Zhen-Yu Sci Rep Article Excess fat accumulation has been observed widely in farmed fish; therefore, efficient lipid-lowering factors have obtained high attention in the current fish nutrition studies. Dietary L-carnitine can increase fatty acid β-oxidation in mammals, but has produced contradictory results in different fish species. To date, the mechanisms of metabolic regulation of L-carnitine in fish have not been fully determined. The present study used zebrafish to investigate the systemic regulation of nutrient metabolism by dietary L-carnitine supplementation. L-carnitine significantly decreased the lipid content in liver and muscle, accompanied by increased concentrations of total and free carnitine in tissues. Meanwhile, L-carnitine enhanced mitochondrial β-oxidation activities and the expression of carnitine palmitoyltransferase 1 mRNA significantly, whereas it depressed the mRNA expression of adipogenesis-related genes. In addition, L-carnitine caused higher glycogen deposition in the fasting state, and increased and decreased the mRNA expressions of gluconeogenesis-related and glycolysis-related genes, respectively. L-carnitine also increased the hepatic expression of mTOR in the feeding state. Taken together, dietary L-carnitine supplementation decreased lipid deposition by increasing mitochondrial fatty acid β-oxidation, and is likely to promote protein synthesis. However, the L-carnitine-enhanced lipid catabolism would cause a decrease in glucose utilization. Therefore, L-carnitine has comprehensive effects on nutrient metabolism in fish. Nature Publishing Group 2017-01-19 /pmc/articles/PMC5244368/ /pubmed/28102299 http://dx.doi.org/10.1038/srep40815 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Li, Jia-Min Li, Ling-Yu Qin, Xun Ning, Li-Jun Lu, Dong-Liang Li, Dong-Liang Zhang, Mei-Ling Wang, Xin Du, Zhen-Yu Systemic regulation of L-carnitine in nutritional metabolism in zebrafish, Danio rerio |
title | Systemic regulation of L-carnitine in nutritional metabolism in zebrafish, Danio rerio |
title_full | Systemic regulation of L-carnitine in nutritional metabolism in zebrafish, Danio rerio |
title_fullStr | Systemic regulation of L-carnitine in nutritional metabolism in zebrafish, Danio rerio |
title_full_unstemmed | Systemic regulation of L-carnitine in nutritional metabolism in zebrafish, Danio rerio |
title_short | Systemic regulation of L-carnitine in nutritional metabolism in zebrafish, Danio rerio |
title_sort | systemic regulation of l-carnitine in nutritional metabolism in zebrafish, danio rerio |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5244368/ https://www.ncbi.nlm.nih.gov/pubmed/28102299 http://dx.doi.org/10.1038/srep40815 |
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