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Role and mechanism of pancreatic β‐cell death in diabetes: The emerging role of autophagy

Pancreatic β‐cell failure resulting from decreased β‐cell mass or dysfunction is the ultimate step towards most types of diabetes. Even if insulin resistance exists, diabetes does not develop unless pancreatic β‐cell function or its adaptation is compromised. Classically, two types of cell death (ap...

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Detalles Bibliográficos
Autores principales: Kim, Kyoung‐Ah, Lee, Myung‐Shik
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4014885/
https://www.ncbi.nlm.nih.gov/pubmed/24843437
http://dx.doi.org/10.1111/j.2040-1124.2010.00054.x
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author Kim, Kyoung‐Ah
Lee, Myung‐Shik
author_facet Kim, Kyoung‐Ah
Lee, Myung‐Shik
author_sort Kim, Kyoung‐Ah
collection PubMed
description Pancreatic β‐cell failure resulting from decreased β‐cell mass or dysfunction is the ultimate step towards most types of diabetes. Even if insulin resistance exists, diabetes does not develop unless pancreatic β‐cell function or its adaptation is compromised. Classically, two types of cell death (apoptosis and necrosis) have been studied in the diabetes field. Recently, a third type of cell death (autophagy, sometimes called type 2 programmed cell death in comparison with apoptosis, type 1 programmed cell death) and its pathophysiological role have been recognized and are being investigated. In the present review, we will discuss the role of various types of cell death in the development of type 1 and type 2 diabetes. Specifically, we will briefly cover recent progress regarding the role of autophagy in diabetes, which is becoming a hot topic in diabetes and metabolism. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.0054.x, 2010)
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spelling pubmed-40148852014-05-19 Role and mechanism of pancreatic β‐cell death in diabetes: The emerging role of autophagy Kim, Kyoung‐Ah Lee, Myung‐Shik J Diabetes Investig Review Article Pancreatic β‐cell failure resulting from decreased β‐cell mass or dysfunction is the ultimate step towards most types of diabetes. Even if insulin resistance exists, diabetes does not develop unless pancreatic β‐cell function or its adaptation is compromised. Classically, two types of cell death (apoptosis and necrosis) have been studied in the diabetes field. Recently, a third type of cell death (autophagy, sometimes called type 2 programmed cell death in comparison with apoptosis, type 1 programmed cell death) and its pathophysiological role have been recognized and are being investigated. In the present review, we will discuss the role of various types of cell death in the development of type 1 and type 2 diabetes. Specifically, we will briefly cover recent progress regarding the role of autophagy in diabetes, which is becoming a hot topic in diabetes and metabolism. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.0054.x, 2010) Blackwell Publishing Ltd 2010-12-03 2010-12-03 /pmc/articles/PMC4014885/ /pubmed/24843437 http://dx.doi.org/10.1111/j.2040-1124.2010.00054.x Text en © 2010 Asian Association for the Study of Diabetes and Blackwell Publishing Asia Pty Ltd
spellingShingle Review Article
Kim, Kyoung‐Ah
Lee, Myung‐Shik
Role and mechanism of pancreatic β‐cell death in diabetes: The emerging role of autophagy
title Role and mechanism of pancreatic β‐cell death in diabetes: The emerging role of autophagy
title_full Role and mechanism of pancreatic β‐cell death in diabetes: The emerging role of autophagy
title_fullStr Role and mechanism of pancreatic β‐cell death in diabetes: The emerging role of autophagy
title_full_unstemmed Role and mechanism of pancreatic β‐cell death in diabetes: The emerging role of autophagy
title_short Role and mechanism of pancreatic β‐cell death in diabetes: The emerging role of autophagy
title_sort role and mechanism of pancreatic β‐cell death in diabetes: the emerging role of autophagy
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4014885/
https://www.ncbi.nlm.nih.gov/pubmed/24843437
http://dx.doi.org/10.1111/j.2040-1124.2010.00054.x
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