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Electroacupuncture inhibits weight gain in diet-induced obese rats by activating hypothalamicLKB1-AMPK signaling
BACKGROUND: Electroacupuncture (EA) is reported to be an effective treatment for obesity, but its mechanism is unclear. This study aimed to investigate the relationship between hypothalamic LKB1-AMPK-ACC signaling and EA. METHODS: Fifty male Sprague–Dawley rats were divided into two groups fed eithe...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4485871/ https://www.ncbi.nlm.nih.gov/pubmed/25963634 http://dx.doi.org/10.1186/s12906-015-0667-7 |
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author | Xu, Jing Chen, Liang Tang, Lewei Chang, Le Liu, Si Tan, Jinfeng Chen, Yinglong Ren, Yulan Liang, Fanrong Cui, Jin |
author_facet | Xu, Jing Chen, Liang Tang, Lewei Chang, Le Liu, Si Tan, Jinfeng Chen, Yinglong Ren, Yulan Liang, Fanrong Cui, Jin |
author_sort | Xu, Jing |
collection | PubMed |
description | BACKGROUND: Electroacupuncture (EA) is reported to be an effective treatment for obesity, but its mechanism is unclear. This study aimed to investigate the relationship between hypothalamic LKB1-AMPK-ACC signaling and EA. METHODS: Fifty male Sprague–Dawley rats were divided into two groups fed either chow (chow-fed group) or high-fat diet (HF group). After 4 weeks of feeding, obese rats in the HF group (defined as weighing 20 % or more than rats in the chow-fed group) were randomly allocated into an EA or Diet-induced obesity (DIO) group. The EA group was given EA on bilateral ST25–ST36 for 4 weeks, while the DIO group received no further intervention. Body weight of the chow-fed, DIO, and EA groups were measured weekly. mRNA and protein levels of the hypothalamic LKB1-AMPK-ACC signaling pathway were detected using real-time (RT)-PCR and western blot, respectively. RESULTS: After 4 weeks of EA treatment, the weight growth trend of rats in the EA group was inhibited compared with those in the DIO group. RT-PCR and western blotting showed that EA upregulated the transcription of Adenosine 5′-monophosphate -activated protein kinase α2 (AMPKα2), promoted protein expression of Liver kinase B1 (LKB1) and AMPKα1, and inhibited acetyl-CoA carboxylase (ACC) protein expression in the hypothalamus. CONCLUSIONS: This study suggests that hypothalamic LKB1-AMPK-ACC signaling plays an important role in EA treatment for obesity. |
format | Online Article Text |
id | pubmed-4485871 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-44858712015-07-01 Electroacupuncture inhibits weight gain in diet-induced obese rats by activating hypothalamicLKB1-AMPK signaling Xu, Jing Chen, Liang Tang, Lewei Chang, Le Liu, Si Tan, Jinfeng Chen, Yinglong Ren, Yulan Liang, Fanrong Cui, Jin BMC Complement Altern Med Research Article BACKGROUND: Electroacupuncture (EA) is reported to be an effective treatment for obesity, but its mechanism is unclear. This study aimed to investigate the relationship between hypothalamic LKB1-AMPK-ACC signaling and EA. METHODS: Fifty male Sprague–Dawley rats were divided into two groups fed either chow (chow-fed group) or high-fat diet (HF group). After 4 weeks of feeding, obese rats in the HF group (defined as weighing 20 % or more than rats in the chow-fed group) were randomly allocated into an EA or Diet-induced obesity (DIO) group. The EA group was given EA on bilateral ST25–ST36 for 4 weeks, while the DIO group received no further intervention. Body weight of the chow-fed, DIO, and EA groups were measured weekly. mRNA and protein levels of the hypothalamic LKB1-AMPK-ACC signaling pathway were detected using real-time (RT)-PCR and western blot, respectively. RESULTS: After 4 weeks of EA treatment, the weight growth trend of rats in the EA group was inhibited compared with those in the DIO group. RT-PCR and western blotting showed that EA upregulated the transcription of Adenosine 5′-monophosphate -activated protein kinase α2 (AMPKα2), promoted protein expression of Liver kinase B1 (LKB1) and AMPKα1, and inhibited acetyl-CoA carboxylase (ACC) protein expression in the hypothalamus. CONCLUSIONS: This study suggests that hypothalamic LKB1-AMPK-ACC signaling plays an important role in EA treatment for obesity. BioMed Central 2015-05-12 /pmc/articles/PMC4485871/ /pubmed/25963634 http://dx.doi.org/10.1186/s12906-015-0667-7 Text en © Xu et al. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), 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 Xu, Jing Chen, Liang Tang, Lewei Chang, Le Liu, Si Tan, Jinfeng Chen, Yinglong Ren, Yulan Liang, Fanrong Cui, Jin Electroacupuncture inhibits weight gain in diet-induced obese rats by activating hypothalamicLKB1-AMPK signaling |
title | Electroacupuncture inhibits weight gain in diet-induced obese rats by activating hypothalamicLKB1-AMPK signaling |
title_full | Electroacupuncture inhibits weight gain in diet-induced obese rats by activating hypothalamicLKB1-AMPK signaling |
title_fullStr | Electroacupuncture inhibits weight gain in diet-induced obese rats by activating hypothalamicLKB1-AMPK signaling |
title_full_unstemmed | Electroacupuncture inhibits weight gain in diet-induced obese rats by activating hypothalamicLKB1-AMPK signaling |
title_short | Electroacupuncture inhibits weight gain in diet-induced obese rats by activating hypothalamicLKB1-AMPK signaling |
title_sort | electroacupuncture inhibits weight gain in diet-induced obese rats by activating hypothalamiclkb1-ampk signaling |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4485871/ https://www.ncbi.nlm.nih.gov/pubmed/25963634 http://dx.doi.org/10.1186/s12906-015-0667-7 |
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