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Palmitoleate inhibits insulin transcription by activating the ERK1/2 pathway in rat pancreatic β-cells
The aim of the present study was to evaluate the effects of palmitoleate on insulin secretion and insulin mRNA levels, and to investigate the transcriptional regulation of insulin. INS-1 rat insulinoma cells were treated with palmitoleate in the presence of high glucose, and the amount of secreted i...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5450653/ https://www.ncbi.nlm.nih.gov/pubmed/28587345 http://dx.doi.org/10.3892/etm.2017.4344 |
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author | Yang, Yumei Gong, Liangliang |
author_facet | Yang, Yumei Gong, Liangliang |
author_sort | Yang, Yumei |
collection | PubMed |
description | The aim of the present study was to evaluate the effects of palmitoleate on insulin secretion and insulin mRNA levels, and to investigate the transcriptional regulation of insulin. INS-1 rat insulinoma cells were treated with palmitoleate in the presence of high glucose, and the amount of secreted insulin was measured via radioimmunoassay. Reverse transcription-quantitative polymerase chain reaction was performed to evaluate the mRNA levels of insulin and pancreatic and duodenal homeobox 1 (PDX1) under palmitoleate treatment. The levels of PDX1, peroxisome proliferator-activated receptor gamma (PPARG), extracellular signal-regulated kinase (ERK)1/2 and phosphorylated ERK1/2 were measured using western blot analysis. Low concentrations of palmitoleate significantly induced insulin secretion (P=0.024), whereas the mRNA levels of insulin and PDX1 were markedly reduced. However, the inhibitory effects were reversed with the addition of U0126, suggesting that the ERK1/2-mediated pathway may be the underlying mechanism responsible for palmitoleate-induced downregulation of insulin mRNA. Exposure of INS-1 cells to high glucose significantly increased the phosphorylation of ERK1/2 (P=0.039), which was further enhanced by palmitoleate (P=0.025). Exposure of INS-1 cells to high glucose significantly decreased PPARG (P=0.001), which was further decreased by the addition of palmitoleate. U0126 was able to reverse the palmitoleate-induced effects. In conclusion, the present study suggested that palmitoleate may induce insulin secretion and inhibit insulin mRNA expression in pancreatic β-cells. |
format | Online Article Text |
id | pubmed-5450653 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-54506532017-06-05 Palmitoleate inhibits insulin transcription by activating the ERK1/2 pathway in rat pancreatic β-cells Yang, Yumei Gong, Liangliang Exp Ther Med Articles The aim of the present study was to evaluate the effects of palmitoleate on insulin secretion and insulin mRNA levels, and to investigate the transcriptional regulation of insulin. INS-1 rat insulinoma cells were treated with palmitoleate in the presence of high glucose, and the amount of secreted insulin was measured via radioimmunoassay. Reverse transcription-quantitative polymerase chain reaction was performed to evaluate the mRNA levels of insulin and pancreatic and duodenal homeobox 1 (PDX1) under palmitoleate treatment. The levels of PDX1, peroxisome proliferator-activated receptor gamma (PPARG), extracellular signal-regulated kinase (ERK)1/2 and phosphorylated ERK1/2 were measured using western blot analysis. Low concentrations of palmitoleate significantly induced insulin secretion (P=0.024), whereas the mRNA levels of insulin and PDX1 were markedly reduced. However, the inhibitory effects were reversed with the addition of U0126, suggesting that the ERK1/2-mediated pathway may be the underlying mechanism responsible for palmitoleate-induced downregulation of insulin mRNA. Exposure of INS-1 cells to high glucose significantly increased the phosphorylation of ERK1/2 (P=0.039), which was further enhanced by palmitoleate (P=0.025). Exposure of INS-1 cells to high glucose significantly decreased PPARG (P=0.001), which was further decreased by the addition of palmitoleate. U0126 was able to reverse the palmitoleate-induced effects. In conclusion, the present study suggested that palmitoleate may induce insulin secretion and inhibit insulin mRNA expression in pancreatic β-cells. D.A. Spandidos 2017-06 2017-04-18 /pmc/articles/PMC5450653/ /pubmed/28587345 http://dx.doi.org/10.3892/etm.2017.4344 Text en Copyright: © Yang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Yang, Yumei Gong, Liangliang Palmitoleate inhibits insulin transcription by activating the ERK1/2 pathway in rat pancreatic β-cells |
title | Palmitoleate inhibits insulin transcription by activating the ERK1/2 pathway in rat pancreatic β-cells |
title_full | Palmitoleate inhibits insulin transcription by activating the ERK1/2 pathway in rat pancreatic β-cells |
title_fullStr | Palmitoleate inhibits insulin transcription by activating the ERK1/2 pathway in rat pancreatic β-cells |
title_full_unstemmed | Palmitoleate inhibits insulin transcription by activating the ERK1/2 pathway in rat pancreatic β-cells |
title_short | Palmitoleate inhibits insulin transcription by activating the ERK1/2 pathway in rat pancreatic β-cells |
title_sort | palmitoleate inhibits insulin transcription by activating the erk1/2 pathway in rat pancreatic β-cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5450653/ https://www.ncbi.nlm.nih.gov/pubmed/28587345 http://dx.doi.org/10.3892/etm.2017.4344 |
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