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Curcumin inhibits lipolysis via suppression of ER stress in adipose tissue and prevents hepatic insulin resistance
Curcumin is natural polyphenol with beneficial effects on lipid and glucose metabolism and this study aimed to investigate the effects of curcumin on lipolysis and hepatic insulin resistance. Endoplasmic reticulum (ER) stress and lipolysis signaling in adipose and FFA influx, lipid deposits, and glu...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Biochemistry and Molecular Biology
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918853/ https://www.ncbi.nlm.nih.gov/pubmed/27220352 http://dx.doi.org/10.1194/jlr.M067397 |
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author | Wang, Lulu Zhang, Bangling Huang, Fang Liu, Baolin Xie, Yuan |
author_facet | Wang, Lulu Zhang, Bangling Huang, Fang Liu, Baolin Xie, Yuan |
author_sort | Wang, Lulu |
collection | PubMed |
description | Curcumin is natural polyphenol with beneficial effects on lipid and glucose metabolism and this study aimed to investigate the effects of curcumin on lipolysis and hepatic insulin resistance. Endoplasmic reticulum (ER) stress and lipolysis signaling in adipose and FFA influx, lipid deposits, and glucose production in liver were examined. Palmitate challenge and high-fat diet feeding evoked ER stress-associated lipolysis with cAMP accumulation in adipose tissue. Curcumin treatment inhibited adipose tissue ER stress by dephosphorylation of inositol-requiring enzyme 1α and eukaryotic initiation factor 2α and reduced cAMP accumulation by preserving phosphodiesterase 3B induction. Knockdown of mitogen-activated protein kinase α1/2α with siRNAs diminished such effects of curcumin. As a result from downregulation of cAMP, curcumin blocked protein kinase (PK)A/hormone-sensitive lipase lipolysis signaling, and thereby reduced glycerol and FFA release from adipose tissue. Curcumin reduced FFA influx into the liver by blocking FFA trafficking, and then prevented diacylglycerol deposits and PKCε translocation in the liver, resultantly improving insulin action in the suppression of hepatic gluconeogenesis. Curcumin decreased adipose lipolysis by attenuating ER stress through the cAMP/PKA pathway, reduced FFA influx into the liver by blocking FFA trafficking, and thereby improved insulin sensitivity to inhibit hepatic glucose production. These findings suggested a novel pathway of curcumin to prevent lipid deposits and insulin resistance in liver by beneficial regulation of adipose function. |
format | Online Article Text |
id | pubmed-4918853 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | The American Society for Biochemistry and Molecular Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-49188532017-07-01 Curcumin inhibits lipolysis via suppression of ER stress in adipose tissue and prevents hepatic insulin resistance Wang, Lulu Zhang, Bangling Huang, Fang Liu, Baolin Xie, Yuan J Lipid Res Research Articles Curcumin is natural polyphenol with beneficial effects on lipid and glucose metabolism and this study aimed to investigate the effects of curcumin on lipolysis and hepatic insulin resistance. Endoplasmic reticulum (ER) stress and lipolysis signaling in adipose and FFA influx, lipid deposits, and glucose production in liver were examined. Palmitate challenge and high-fat diet feeding evoked ER stress-associated lipolysis with cAMP accumulation in adipose tissue. Curcumin treatment inhibited adipose tissue ER stress by dephosphorylation of inositol-requiring enzyme 1α and eukaryotic initiation factor 2α and reduced cAMP accumulation by preserving phosphodiesterase 3B induction. Knockdown of mitogen-activated protein kinase α1/2α with siRNAs diminished such effects of curcumin. As a result from downregulation of cAMP, curcumin blocked protein kinase (PK)A/hormone-sensitive lipase lipolysis signaling, and thereby reduced glycerol and FFA release from adipose tissue. Curcumin reduced FFA influx into the liver by blocking FFA trafficking, and then prevented diacylglycerol deposits and PKCε translocation in the liver, resultantly improving insulin action in the suppression of hepatic gluconeogenesis. Curcumin decreased adipose lipolysis by attenuating ER stress through the cAMP/PKA pathway, reduced FFA influx into the liver by blocking FFA trafficking, and thereby improved insulin sensitivity to inhibit hepatic glucose production. These findings suggested a novel pathway of curcumin to prevent lipid deposits and insulin resistance in liver by beneficial regulation of adipose function. The American Society for Biochemistry and Molecular Biology 2016-07 /pmc/articles/PMC4918853/ /pubmed/27220352 http://dx.doi.org/10.1194/jlr.M067397 Text en Copyright © 2016 by the American Society for Biochemistry and Molecular Biology, Inc. http://creativecommons.org/licenses/by/4.0/ Author’s Choice—Final version free via Creative Commons CC-BY license. |
spellingShingle | Research Articles Wang, Lulu Zhang, Bangling Huang, Fang Liu, Baolin Xie, Yuan Curcumin inhibits lipolysis via suppression of ER stress in adipose tissue and prevents hepatic insulin resistance |
title | Curcumin inhibits lipolysis via suppression of ER stress in adipose tissue and prevents hepatic insulin resistance |
title_full | Curcumin inhibits lipolysis via suppression of ER stress in adipose tissue and prevents hepatic insulin resistance |
title_fullStr | Curcumin inhibits lipolysis via suppression of ER stress in adipose tissue and prevents hepatic insulin resistance |
title_full_unstemmed | Curcumin inhibits lipolysis via suppression of ER stress in adipose tissue and prevents hepatic insulin resistance |
title_short | Curcumin inhibits lipolysis via suppression of ER stress in adipose tissue and prevents hepatic insulin resistance |
title_sort | curcumin inhibits lipolysis via suppression of er stress in adipose tissue and prevents hepatic insulin resistance |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918853/ https://www.ncbi.nlm.nih.gov/pubmed/27220352 http://dx.doi.org/10.1194/jlr.M067397 |
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