Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Food Science and Technology (Campinas) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100712 |
Resumo: | Abstract Vitamin D (VD) was reported to play protective roles in skeletal muscle. This study aimed to explore whether endoplasmic reticulum (ER) stress inhibition is associated with the protective effects of VD/VD receptor (VDR) signaling on skeletal muscle functions. C2C12 skeletal muscle cells were treated with palmitic acid (PA) and then incubated with different concentrations of 1,25-(OH)2-vitamin D3 (VD3), and we found that VD3 improved the impaired cell viability induced by PA and increased VDR expression in a dose-dependent manner. Then 100 nM VD3 treatment and VDR overexpression both ameliorated PA-induced ER stress, apoptosis, inflammation and glucose uptake inhibition in C2C12 myocytes. Furthermore, VDR knockdown reversed the protective effects of VD3 on C2C12 cell functions. Additionally, PA-treated C2C12 cells were treated with VD3 alone or together with AMPK signaling inhibitor Compound C. VD3 promoted phosphorylation of AMPK and SIRT1 expression, while Compound C reversed these effects and abolished the protective effects of VD3 in C2C12 cells. High-fat diet (HFD)-fed mice were treated with VD3, and VD3 alleviated skeletal muscle loss and insulin resistance in mice. In conclusion, VD inhibited AMPK/SIRT1-mediated ER stress by increasing VDR expression, and further ameliorated skeletal muscle loss and insulin resistance in mice. |
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Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in miceVDVDRskeletal muscle lossinsulin resistanceAMPK/SIRT1 signaling pathwayendoplasmic reticulum stressAbstract Vitamin D (VD) was reported to play protective roles in skeletal muscle. This study aimed to explore whether endoplasmic reticulum (ER) stress inhibition is associated with the protective effects of VD/VD receptor (VDR) signaling on skeletal muscle functions. C2C12 skeletal muscle cells were treated with palmitic acid (PA) and then incubated with different concentrations of 1,25-(OH)2-vitamin D3 (VD3), and we found that VD3 improved the impaired cell viability induced by PA and increased VDR expression in a dose-dependent manner. Then 100 nM VD3 treatment and VDR overexpression both ameliorated PA-induced ER stress, apoptosis, inflammation and glucose uptake inhibition in C2C12 myocytes. Furthermore, VDR knockdown reversed the protective effects of VD3 on C2C12 cell functions. Additionally, PA-treated C2C12 cells were treated with VD3 alone or together with AMPK signaling inhibitor Compound C. VD3 promoted phosphorylation of AMPK and SIRT1 expression, while Compound C reversed these effects and abolished the protective effects of VD3 in C2C12 cells. High-fat diet (HFD)-fed mice were treated with VD3, and VD3 alleviated skeletal muscle loss and insulin resistance in mice. In conclusion, VD inhibited AMPK/SIRT1-mediated ER stress by increasing VDR expression, and further ameliorated skeletal muscle loss and insulin resistance in mice.Sociedade Brasileira de Ciência e Tecnologia de Alimentos2022-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100712Food Science and Technology v.42 2022reponame:Food Science and Technology (Campinas)instname:Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA)instacron:SBCTA10.1590/fst.47921info:eu-repo/semantics/openAccessLI,AijuanSHEN,PengchengLIU,SijiaWANG,JiaoZENG,JingruDU,Chunpingeng2022-02-23T00:00:00Zoai:scielo:S0101-20612022000100712Revistahttp://www.scielo.br/ctaONGhttps://old.scielo.br/oai/scielo-oai.php||revista@sbcta.org.br1678-457X0101-2061opendoar:2022-02-23T00:00Food Science and Technology (Campinas) - Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA)false |
dc.title.none.fl_str_mv |
Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice |
title |
Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice |
spellingShingle |
Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice LI,Aijuan VD VDR skeletal muscle loss insulin resistance AMPK/SIRT1 signaling pathway endoplasmic reticulum stress |
title_short |
Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice |
title_full |
Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice |
title_fullStr |
Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice |
title_full_unstemmed |
Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice |
title_sort |
Vitamin D alleviates skeletal muscle loss and insulin resistance by inducing vitamin D receptor expression and regulating the AMPK/SIRT1 signaling pathway in mice |
author |
LI,Aijuan |
author_facet |
LI,Aijuan SHEN,Pengcheng LIU,Sijia WANG,Jiao ZENG,Jingru DU,Chunping |
author_role |
author |
author2 |
SHEN,Pengcheng LIU,Sijia WANG,Jiao ZENG,Jingru DU,Chunping |
author2_role |
author author author author author |
dc.contributor.author.fl_str_mv |
LI,Aijuan SHEN,Pengcheng LIU,Sijia WANG,Jiao ZENG,Jingru DU,Chunping |
dc.subject.por.fl_str_mv |
VD VDR skeletal muscle loss insulin resistance AMPK/SIRT1 signaling pathway endoplasmic reticulum stress |
topic |
VD VDR skeletal muscle loss insulin resistance AMPK/SIRT1 signaling pathway endoplasmic reticulum stress |
description |
Abstract Vitamin D (VD) was reported to play protective roles in skeletal muscle. This study aimed to explore whether endoplasmic reticulum (ER) stress inhibition is associated with the protective effects of VD/VD receptor (VDR) signaling on skeletal muscle functions. C2C12 skeletal muscle cells were treated with palmitic acid (PA) and then incubated with different concentrations of 1,25-(OH)2-vitamin D3 (VD3), and we found that VD3 improved the impaired cell viability induced by PA and increased VDR expression in a dose-dependent manner. Then 100 nM VD3 treatment and VDR overexpression both ameliorated PA-induced ER stress, apoptosis, inflammation and glucose uptake inhibition in C2C12 myocytes. Furthermore, VDR knockdown reversed the protective effects of VD3 on C2C12 cell functions. Additionally, PA-treated C2C12 cells were treated with VD3 alone or together with AMPK signaling inhibitor Compound C. VD3 promoted phosphorylation of AMPK and SIRT1 expression, while Compound C reversed these effects and abolished the protective effects of VD3 in C2C12 cells. High-fat diet (HFD)-fed mice were treated with VD3, and VD3 alleviated skeletal muscle loss and insulin resistance in mice. In conclusion, VD inhibited AMPK/SIRT1-mediated ER stress by increasing VDR expression, and further ameliorated skeletal muscle loss and insulin resistance in mice. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100712 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100712 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/fst.47921 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Ciência e Tecnologia de Alimentos |
publisher.none.fl_str_mv |
Sociedade Brasileira de Ciência e Tecnologia de Alimentos |
dc.source.none.fl_str_mv |
Food Science and Technology v.42 2022 reponame:Food Science and Technology (Campinas) instname:Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA) instacron:SBCTA |
instname_str |
Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA) |
instacron_str |
SBCTA |
institution |
SBCTA |
reponame_str |
Food Science and Technology (Campinas) |
collection |
Food Science and Technology (Campinas) |
repository.name.fl_str_mv |
Food Science and Technology (Campinas) - Sociedade Brasileira de Ciência e Tecnologia de Alimentos (SBCTA) |
repository.mail.fl_str_mv |
||revista@sbcta.org.br |
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1752126332519579648 |