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Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review
Insulin resistance and pancreatic beta cell dysfunction are major contributors to the pathogenesis of diabetes. Various conditions play a role in the pathogenesis of pancreatic beta cell dysfunction and are correlated with endoplasmic reticulum (ER) stress. Pancreatic beta cells are susceptible to E...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303544/ https://www.ncbi.nlm.nih.gov/pubmed/22474424 http://dx.doi.org/10.1155/2012/509437 |
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author | Kim, Mi-Kyung Kim, Hye-Soon Lee, In-Kyu Park, Keun-Gyu |
author_facet | Kim, Mi-Kyung Kim, Hye-Soon Lee, In-Kyu Park, Keun-Gyu |
author_sort | Kim, Mi-Kyung |
collection | PubMed |
description | Insulin resistance and pancreatic beta cell dysfunction are major contributors to the pathogenesis of diabetes. Various conditions play a role in the pathogenesis of pancreatic beta cell dysfunction and are correlated with endoplasmic reticulum (ER) stress. Pancreatic beta cells are susceptible to ER stress. Many studies have shown that increased ER stress induces pancreatic beta cell dysfunction and diabetes mellitus using genetic models of ER stress and by various stimuli. There are many reports indicating that ER stress plays an important role in the impairment of insulin biosynthesis, suggesting that reduction of ER stress could be a therapeutic target for diabetes. In this paper, we reviewed the relationship between ER stress and diabetes and how ER stress controls insulin biosynthesis. |
format | Online Article Text |
id | pubmed-3303544 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-33035442012-04-03 Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review Kim, Mi-Kyung Kim, Hye-Soon Lee, In-Kyu Park, Keun-Gyu Exp Diabetes Res Review Article Insulin resistance and pancreatic beta cell dysfunction are major contributors to the pathogenesis of diabetes. Various conditions play a role in the pathogenesis of pancreatic beta cell dysfunction and are correlated with endoplasmic reticulum (ER) stress. Pancreatic beta cells are susceptible to ER stress. Many studies have shown that increased ER stress induces pancreatic beta cell dysfunction and diabetes mellitus using genetic models of ER stress and by various stimuli. There are many reports indicating that ER stress plays an important role in the impairment of insulin biosynthesis, suggesting that reduction of ER stress could be a therapeutic target for diabetes. In this paper, we reviewed the relationship between ER stress and diabetes and how ER stress controls insulin biosynthesis. Hindawi Publishing Corporation 2012 2012-03-05 /pmc/articles/PMC3303544/ /pubmed/22474424 http://dx.doi.org/10.1155/2012/509437 Text en Copyright © 2012 Mi-Kyung Kim et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Kim, Mi-Kyung Kim, Hye-Soon Lee, In-Kyu Park, Keun-Gyu Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review |
title | Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review |
title_full | Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review |
title_fullStr | Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review |
title_full_unstemmed | Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review |
title_short | Endoplasmic Reticulum Stress and Insulin Biosynthesis: A Review |
title_sort | endoplasmic reticulum stress and insulin biosynthesis: a review |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3303544/ https://www.ncbi.nlm.nih.gov/pubmed/22474424 http://dx.doi.org/10.1155/2012/509437 |
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