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Diversity of pathophysiology in type 2 diabetes shown by islet pathology
The etiology of type 2 diabetes is multifactorial, in which environmental and genetic factors are involved to varying degrees. This suggests that its pathophysiology might vary depending on the individuals. Knowledge of the differences is critical, because these differences are directly linked to th...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8756316/ https://www.ncbi.nlm.nih.gov/pubmed/34562302 http://dx.doi.org/10.1111/jdi.13679 |
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author | Mizukami, Hiroki Kudoh, Kazuhiro |
author_facet | Mizukami, Hiroki Kudoh, Kazuhiro |
author_sort | Mizukami, Hiroki |
collection | PubMed |
description | The etiology of type 2 diabetes is multifactorial, in which environmental and genetic factors are involved to varying degrees. This suggests that its pathophysiology might vary depending on the individuals. Knowledge of the differences is critical, because these differences are directly linked to the care and treatment of the patients. Recent studies have attempted to carry out subclassifications of type 2 diabetes based on clinical and genetic differences. However, there is no pathological evidence to support these subclassifications. The pathophysiology of type 2 diabetes is generally divided into insulin resistance in peripheral tissues and pancreatic islet dysfunction. Among them, islet dysfunction causes a deficit in insulin secretion from β‐cells. In particular, a deficit in insulin secretion is ascribed to a combination of disruption of the insulin secretory machinery and a decrease in β‐cell volume in type 2 diabetes. Recent research has suggested that transdifferentiation and dedifferentiation are involved in the decrease in β‐cell volume, and that it might change dynamically depending on the glucose metabolic state. However, it is possible that the numbers of islet cells are decreased in type 2 diabetes. In particular, the loss of endocrine cells due to islet amyloid deposits is an important pathological change in type 2 diabetes in humans. These results show that pathological changes of the islets can be different in each individuals with type 2 diabetes and reflect each pathophysiology, which is useful in establishing further subclassifications and developing tailor‐made therapies for type 2 diabetes. |
format | Online Article Text |
id | pubmed-8756316 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-87563162022-01-19 Diversity of pathophysiology in type 2 diabetes shown by islet pathology Mizukami, Hiroki Kudoh, Kazuhiro J Diabetes Investig Review Article The etiology of type 2 diabetes is multifactorial, in which environmental and genetic factors are involved to varying degrees. This suggests that its pathophysiology might vary depending on the individuals. Knowledge of the differences is critical, because these differences are directly linked to the care and treatment of the patients. Recent studies have attempted to carry out subclassifications of type 2 diabetes based on clinical and genetic differences. However, there is no pathological evidence to support these subclassifications. The pathophysiology of type 2 diabetes is generally divided into insulin resistance in peripheral tissues and pancreatic islet dysfunction. Among them, islet dysfunction causes a deficit in insulin secretion from β‐cells. In particular, a deficit in insulin secretion is ascribed to a combination of disruption of the insulin secretory machinery and a decrease in β‐cell volume in type 2 diabetes. Recent research has suggested that transdifferentiation and dedifferentiation are involved in the decrease in β‐cell volume, and that it might change dynamically depending on the glucose metabolic state. However, it is possible that the numbers of islet cells are decreased in type 2 diabetes. In particular, the loss of endocrine cells due to islet amyloid deposits is an important pathological change in type 2 diabetes in humans. These results show that pathological changes of the islets can be different in each individuals with type 2 diabetes and reflect each pathophysiology, which is useful in establishing further subclassifications and developing tailor‐made therapies for type 2 diabetes. John Wiley and Sons Inc. 2021-10-18 2022-01 /pmc/articles/PMC8756316/ /pubmed/34562302 http://dx.doi.org/10.1111/jdi.13679 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-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, 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 | Review Article Mizukami, Hiroki Kudoh, Kazuhiro Diversity of pathophysiology in type 2 diabetes shown by islet pathology |
title | Diversity of pathophysiology in type 2 diabetes shown by islet pathology |
title_full | Diversity of pathophysiology in type 2 diabetes shown by islet pathology |
title_fullStr | Diversity of pathophysiology in type 2 diabetes shown by islet pathology |
title_full_unstemmed | Diversity of pathophysiology in type 2 diabetes shown by islet pathology |
title_short | Diversity of pathophysiology in type 2 diabetes shown by islet pathology |
title_sort | diversity of pathophysiology in type 2 diabetes shown by islet pathology |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8756316/ https://www.ncbi.nlm.nih.gov/pubmed/34562302 http://dx.doi.org/10.1111/jdi.13679 |
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