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Supplementation with conjugated linoeic acid decreases pig back fat deposition by inducing adipocyte apoptosis

BACKGROUND: Conjugated linoleic acid (CLA), a C18 fatty acid with conjugated double bonds, has been shown to serve as a powerful anti-obesity agent by several research groups, although the precise mechanism remains elusive. Previous studies showed that CLA induced apoptosis in 3T3-L1 cells and in mi...

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Autores principales: Qi, Renli, Yang, Feiyun, Huang, Jinxiu, Peng, Han, Liu, Yan, Liu, Zuohua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074849/
https://www.ncbi.nlm.nih.gov/pubmed/24969229
http://dx.doi.org/10.1186/1746-6148-10-141
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author Qi, Renli
Yang, Feiyun
Huang, Jinxiu
Peng, Han
Liu, Yan
Liu, Zuohua
author_facet Qi, Renli
Yang, Feiyun
Huang, Jinxiu
Peng, Han
Liu, Yan
Liu, Zuohua
author_sort Qi, Renli
collection PubMed
description BACKGROUND: Conjugated linoleic acid (CLA), a C18 fatty acid with conjugated double bonds, has been shown to serve as a powerful anti-obesity agent by several research groups, although the precise mechanism remains elusive. Previous studies showed that CLA induced apoptosis in 3T3-L1 cells and in mice. The aim of this research was to clarify the role of CLA in adipocyte apoptosis in pigs, a relevant model for obesity research. RESULTS: Our results clearly show that back fat deposition of CLA-fed pigs was significantly lower than that of pigs in the control group. Moreover, some typical apoptotic cells were observed among the adipocytes of CLA-fed pigs. Furthermore, the CLA-fed pigs had reduced expression of the anti-apoptosis factor Bcl-2 and increased expression of the pro-apoptosis factors Bax and P53. Subsequently, increased cytochrome C was released from the mitochondria to the endochylema, and the caspase cascade was activated, resulting in cellular apoptosis. These results are consistent with the effects of Bcl-2 and Bax in regulating CLA-induced adipocyte apoptosis via the mitochondrial signaling pathway. However, the increased expression of tumor necrosis factor (TNF)-α and its receptor TNFR indicate that the effect of CLA might partly be through the death receptor signaling pathway in adipose cells. CONCLUSIONS: Our study has demonstrated that CLA reduces pig body fat deposition, an outcome that is partly meditated by apoptosis of adipose cells, and that both the mitochondrial pathway and the death receptor pathway are involved in this effect.
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spelling pubmed-40748492014-07-01 Supplementation with conjugated linoeic acid decreases pig back fat deposition by inducing adipocyte apoptosis Qi, Renli Yang, Feiyun Huang, Jinxiu Peng, Han Liu, Yan Liu, Zuohua BMC Vet Res Research Article BACKGROUND: Conjugated linoleic acid (CLA), a C18 fatty acid with conjugated double bonds, has been shown to serve as a powerful anti-obesity agent by several research groups, although the precise mechanism remains elusive. Previous studies showed that CLA induced apoptosis in 3T3-L1 cells and in mice. The aim of this research was to clarify the role of CLA in adipocyte apoptosis in pigs, a relevant model for obesity research. RESULTS: Our results clearly show that back fat deposition of CLA-fed pigs was significantly lower than that of pigs in the control group. Moreover, some typical apoptotic cells were observed among the adipocytes of CLA-fed pigs. Furthermore, the CLA-fed pigs had reduced expression of the anti-apoptosis factor Bcl-2 and increased expression of the pro-apoptosis factors Bax and P53. Subsequently, increased cytochrome C was released from the mitochondria to the endochylema, and the caspase cascade was activated, resulting in cellular apoptosis. These results are consistent with the effects of Bcl-2 and Bax in regulating CLA-induced adipocyte apoptosis via the mitochondrial signaling pathway. However, the increased expression of tumor necrosis factor (TNF)-α and its receptor TNFR indicate that the effect of CLA might partly be through the death receptor signaling pathway in adipose cells. CONCLUSIONS: Our study has demonstrated that CLA reduces pig body fat deposition, an outcome that is partly meditated by apoptosis of adipose cells, and that both the mitochondrial pathway and the death receptor pathway are involved in this effect. BioMed Central 2014-06-26 /pmc/articles/PMC4074849/ /pubmed/24969229 http://dx.doi.org/10.1186/1746-6148-10-141 Text en Copyright © 2014 Qi et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Qi, Renli
Yang, Feiyun
Huang, Jinxiu
Peng, Han
Liu, Yan
Liu, Zuohua
Supplementation with conjugated linoeic acid decreases pig back fat deposition by inducing adipocyte apoptosis
title Supplementation with conjugated linoeic acid decreases pig back fat deposition by inducing adipocyte apoptosis
title_full Supplementation with conjugated linoeic acid decreases pig back fat deposition by inducing adipocyte apoptosis
title_fullStr Supplementation with conjugated linoeic acid decreases pig back fat deposition by inducing adipocyte apoptosis
title_full_unstemmed Supplementation with conjugated linoeic acid decreases pig back fat deposition by inducing adipocyte apoptosis
title_short Supplementation with conjugated linoeic acid decreases pig back fat deposition by inducing adipocyte apoptosis
title_sort supplementation with conjugated linoeic acid decreases pig back fat deposition by inducing adipocyte apoptosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074849/
https://www.ncbi.nlm.nih.gov/pubmed/24969229
http://dx.doi.org/10.1186/1746-6148-10-141
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