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β‐Cell failure in diabetes: Common susceptibility and mechanisms shared between type 1 and type 2 diabetes

Diabetes mellitus is etiologically classified into type 1, type 2 and other types of diabetes. Despite distinct etiologies and pathogenesis of these subtypes, many studies have suggested the presence of shared susceptibilities and underlying mechanisms in β‐cell failure among different types of diab...

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Detalles Bibliográficos
Autores principales: Ikegami, Hiroshi, Babaya, Naru, Noso, Shinsuke
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8409822/
https://www.ncbi.nlm.nih.gov/pubmed/33993642
http://dx.doi.org/10.1111/jdi.13576
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author Ikegami, Hiroshi
Babaya, Naru
Noso, Shinsuke
author_facet Ikegami, Hiroshi
Babaya, Naru
Noso, Shinsuke
author_sort Ikegami, Hiroshi
collection PubMed
description Diabetes mellitus is etiologically classified into type 1, type 2 and other types of diabetes. Despite distinct etiologies and pathogenesis of these subtypes, many studies have suggested the presence of shared susceptibilities and underlying mechanisms in β‐cell failure among different types of diabetes. Understanding these susceptibilities and mechanisms can help in the development of therapeutic strategies regardless of the diabetes subtype. In this review, we discuss recent evidence indicating the shared genetic susceptibilities and common molecular mechanisms between type 1, type 2 and other types of diabetes, and highlight the future prospects as well.
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spelling pubmed-84098222021-09-03 β‐Cell failure in diabetes: Common susceptibility and mechanisms shared between type 1 and type 2 diabetes Ikegami, Hiroshi Babaya, Naru Noso, Shinsuke J Diabetes Investig Review Diabetes mellitus is etiologically classified into type 1, type 2 and other types of diabetes. Despite distinct etiologies and pathogenesis of these subtypes, many studies have suggested the presence of shared susceptibilities and underlying mechanisms in β‐cell failure among different types of diabetes. Understanding these susceptibilities and mechanisms can help in the development of therapeutic strategies regardless of the diabetes subtype. In this review, we discuss recent evidence indicating the shared genetic susceptibilities and common molecular mechanisms between type 1, type 2 and other types of diabetes, and highlight the future prospects as well. John Wiley and Sons Inc. 2021-06-16 2021-09 /pmc/articles/PMC8409822/ /pubmed/33993642 http://dx.doi.org/10.1111/jdi.13576 Text en © 2021 The Authors. Journal of Diabetes Investigation published by Asian Association for the Study of Diabetes (AASD) and John Wiley & Sons Australia, Ltd https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Review
Ikegami, Hiroshi
Babaya, Naru
Noso, Shinsuke
β‐Cell failure in diabetes: Common susceptibility and mechanisms shared between type 1 and type 2 diabetes
title β‐Cell failure in diabetes: Common susceptibility and mechanisms shared between type 1 and type 2 diabetes
title_full β‐Cell failure in diabetes: Common susceptibility and mechanisms shared between type 1 and type 2 diabetes
title_fullStr β‐Cell failure in diabetes: Common susceptibility and mechanisms shared between type 1 and type 2 diabetes
title_full_unstemmed β‐Cell failure in diabetes: Common susceptibility and mechanisms shared between type 1 and type 2 diabetes
title_short β‐Cell failure in diabetes: Common susceptibility and mechanisms shared between type 1 and type 2 diabetes
title_sort β‐cell failure in diabetes: common susceptibility and mechanisms shared between type 1 and type 2 diabetes
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8409822/
https://www.ncbi.nlm.nih.gov/pubmed/33993642
http://dx.doi.org/10.1111/jdi.13576
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