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Induction of remission in diabetes by lowering blood glucose

As diabetes continues to grow as major health problem, there has been great progress in understanding the important role of pancreatic beta-cells in its pathogenesis. Diabetes develops when the normal interplay between insulin secretion and the insulin sensitivity of target tissues is disrupted. Wit...

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Autores principales: Weir, Gordon C., Bonner-Weir, Susan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10318898/
https://www.ncbi.nlm.nih.gov/pubmed/37409234
http://dx.doi.org/10.3389/fendo.2023.1213954
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author Weir, Gordon C.
Bonner-Weir, Susan
author_facet Weir, Gordon C.
Bonner-Weir, Susan
author_sort Weir, Gordon C.
collection PubMed
description As diabetes continues to grow as major health problem, there has been great progress in understanding the important role of pancreatic beta-cells in its pathogenesis. Diabetes develops when the normal interplay between insulin secretion and the insulin sensitivity of target tissues is disrupted. With type 2 diabetes (T2D), glucose levels start to rise when beta-cells are unable to meet the demands of insulin resistance. For type 1 diabetes (T1D) glucose levels rise as beta-cells are killed off by autoimmunity. In both cases the increased glucose levels have a toxic effect on beta-cells. This process, called glucose toxicity, has a major inhibitory effect on insulin secretion. This beta-cell dysfunction can be reversed by therapies that reduce glucose levels. Thus, it is becoming increasingly apparent that an opportunity exists to produce a complete or partial remission for T2D, both of which will provide health benefit.
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spelling pubmed-103188982023-07-05 Induction of remission in diabetes by lowering blood glucose Weir, Gordon C. Bonner-Weir, Susan Front Endocrinol (Lausanne) Endocrinology As diabetes continues to grow as major health problem, there has been great progress in understanding the important role of pancreatic beta-cells in its pathogenesis. Diabetes develops when the normal interplay between insulin secretion and the insulin sensitivity of target tissues is disrupted. With type 2 diabetes (T2D), glucose levels start to rise when beta-cells are unable to meet the demands of insulin resistance. For type 1 diabetes (T1D) glucose levels rise as beta-cells are killed off by autoimmunity. In both cases the increased glucose levels have a toxic effect on beta-cells. This process, called glucose toxicity, has a major inhibitory effect on insulin secretion. This beta-cell dysfunction can be reversed by therapies that reduce glucose levels. Thus, it is becoming increasingly apparent that an opportunity exists to produce a complete or partial remission for T2D, both of which will provide health benefit. Frontiers Media S.A. 2023-06-20 /pmc/articles/PMC10318898/ /pubmed/37409234 http://dx.doi.org/10.3389/fendo.2023.1213954 Text en Copyright © 2023 Weir and Bonner-Weir https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Weir, Gordon C.
Bonner-Weir, Susan
Induction of remission in diabetes by lowering blood glucose
title Induction of remission in diabetes by lowering blood glucose
title_full Induction of remission in diabetes by lowering blood glucose
title_fullStr Induction of remission in diabetes by lowering blood glucose
title_full_unstemmed Induction of remission in diabetes by lowering blood glucose
title_short Induction of remission in diabetes by lowering blood glucose
title_sort induction of remission in diabetes by lowering blood glucose
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10318898/
https://www.ncbi.nlm.nih.gov/pubmed/37409234
http://dx.doi.org/10.3389/fendo.2023.1213954
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