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Berberine increases adipose triglyceride lipase in 3T3-L1 adipocytes through the AMPK pathway
BACKGROUND: Obesity is closely related to the metabolism of triacylglycerol (TG) in adipocytes. Adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) are rate-limiting enzymes that control the hydrolysis of TG. Effects on ATGL and HSL to increase lipolysis may counteract obesity. Ber...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5148888/ https://www.ncbi.nlm.nih.gov/pubmed/27938388 http://dx.doi.org/10.1186/s12944-016-0383-4 |
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author | Jiang, Dongqing Wang, Dianhui Zhuang, Xianghua Wang, Zhanqing Ni, Yihong Chen, Shihong Sun, Fudun |
author_facet | Jiang, Dongqing Wang, Dianhui Zhuang, Xianghua Wang, Zhanqing Ni, Yihong Chen, Shihong Sun, Fudun |
author_sort | Jiang, Dongqing |
collection | PubMed |
description | BACKGROUND: Obesity is closely related to the metabolism of triacylglycerol (TG) in adipocytes. Adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) are rate-limiting enzymes that control the hydrolysis of TG. Effects on ATGL and HSL to increase lipolysis may counteract obesity. Berberine (BBR) is a compound derived from the Chinese medicine plant Coptis chinensis. In the present study we show the effects of BBR on ATGL and HSL and explore the potential underlying mechanisms of these effects. METHODS: The TG content in cells was measured using a colorimetric assay. The expressions of HSL, ATGL and GPAT3 were evaluated by Western-blotting. The expression of ATGL was also evaluated by real-time PCR and radioimmunoassay. Compound C, an inhibitor of AMP-activated protein kinase (AMPK), was used to explore the possible pathway that involved in the effect of BBR on ATGL. RESULTS: TG content of differentiated 3T3-L1 cells was significantly decreased by more than 10% after treated with BBR. In differentiated 3T3-L1 adipocytes, BBR increased the expression of p-HSL and ATGL, and these effects were time-depended (p <0.01). The effect of BBR on ATGL expression could be abolished by Compound C which suggested that AMPK pathway was involved in the effects of BBR on p-HSL and ATGL. CONCLUSIONS: BBR could increase the expression of ATGL and therefore stimulate basal lipolysis in mature adipocytes through the associated mechanisms related to the AMPK pathway. |
format | Online Article Text |
id | pubmed-5148888 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-51488882016-12-16 Berberine increases adipose triglyceride lipase in 3T3-L1 adipocytes through the AMPK pathway Jiang, Dongqing Wang, Dianhui Zhuang, Xianghua Wang, Zhanqing Ni, Yihong Chen, Shihong Sun, Fudun Lipids Health Dis Research BACKGROUND: Obesity is closely related to the metabolism of triacylglycerol (TG) in adipocytes. Adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) are rate-limiting enzymes that control the hydrolysis of TG. Effects on ATGL and HSL to increase lipolysis may counteract obesity. Berberine (BBR) is a compound derived from the Chinese medicine plant Coptis chinensis. In the present study we show the effects of BBR on ATGL and HSL and explore the potential underlying mechanisms of these effects. METHODS: The TG content in cells was measured using a colorimetric assay. The expressions of HSL, ATGL and GPAT3 were evaluated by Western-blotting. The expression of ATGL was also evaluated by real-time PCR and radioimmunoassay. Compound C, an inhibitor of AMP-activated protein kinase (AMPK), was used to explore the possible pathway that involved in the effect of BBR on ATGL. RESULTS: TG content of differentiated 3T3-L1 cells was significantly decreased by more than 10% after treated with BBR. In differentiated 3T3-L1 adipocytes, BBR increased the expression of p-HSL and ATGL, and these effects were time-depended (p <0.01). The effect of BBR on ATGL expression could be abolished by Compound C which suggested that AMPK pathway was involved in the effects of BBR on p-HSL and ATGL. CONCLUSIONS: BBR could increase the expression of ATGL and therefore stimulate basal lipolysis in mature adipocytes through the associated mechanisms related to the AMPK pathway. BioMed Central 2016-12-09 /pmc/articles/PMC5148888/ /pubmed/27938388 http://dx.doi.org/10.1186/s12944-016-0383-4 Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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 Jiang, Dongqing Wang, Dianhui Zhuang, Xianghua Wang, Zhanqing Ni, Yihong Chen, Shihong Sun, Fudun Berberine increases adipose triglyceride lipase in 3T3-L1 adipocytes through the AMPK pathway |
title | Berberine increases adipose triglyceride lipase in 3T3-L1 adipocytes through the AMPK pathway |
title_full | Berberine increases adipose triglyceride lipase in 3T3-L1 adipocytes through the AMPK pathway |
title_fullStr | Berberine increases adipose triglyceride lipase in 3T3-L1 adipocytes through the AMPK pathway |
title_full_unstemmed | Berberine increases adipose triglyceride lipase in 3T3-L1 adipocytes through the AMPK pathway |
title_short | Berberine increases adipose triglyceride lipase in 3T3-L1 adipocytes through the AMPK pathway |
title_sort | berberine increases adipose triglyceride lipase in 3t3-l1 adipocytes through the ampk pathway |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5148888/ https://www.ncbi.nlm.nih.gov/pubmed/27938388 http://dx.doi.org/10.1186/s12944-016-0383-4 |
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