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The stress of starvation: glucocorticoid restraint of beta cell development

Developmental insults during gestation, such as under-nutrition, are known to restrict the number of beta cells that form in the fetal pancreas and are maintained in adulthood, leading to increased risk of type 2 diabetes. There are now substantial data indicating that glucocorticoids mediate this e...

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Detalles Bibliográficos
Autores principales: Matthews, L. C., Hanley, N. A.
Formato: Texto
Lenguaje:English
Publicado: Springer-Verlag 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3017310/
https://www.ncbi.nlm.nih.gov/pubmed/21072627
http://dx.doi.org/10.1007/s00125-010-1963-x
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author Matthews, L. C.
Hanley, N. A.
author_facet Matthews, L. C.
Hanley, N. A.
author_sort Matthews, L. C.
collection PubMed
description Developmental insults during gestation, such as under-nutrition, are known to restrict the number of beta cells that form in the fetal pancreas and are maintained in adulthood, leading to increased risk of type 2 diabetes. There are now substantial data indicating that glucocorticoids mediate this effect of under-nutrition on beta cell mass and that even at physiological levels they restrain fetal beta cell development in utero. There are emerging clues that this occurs downstream of endocrine commitment by neurogenin 3 but prior to terminal beta cell differentiation. Deciphering the precise mechanism will be important as it might unveil new pathways by which to manipulate beta cell mass that could be exploited as novel therapies for patients with diabetes.
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spelling pubmed-30173102011-02-04 The stress of starvation: glucocorticoid restraint of beta cell development Matthews, L. C. Hanley, N. A. Diabetologia Commentary Developmental insults during gestation, such as under-nutrition, are known to restrict the number of beta cells that form in the fetal pancreas and are maintained in adulthood, leading to increased risk of type 2 diabetes. There are now substantial data indicating that glucocorticoids mediate this effect of under-nutrition on beta cell mass and that even at physiological levels they restrain fetal beta cell development in utero. There are emerging clues that this occurs downstream of endocrine commitment by neurogenin 3 but prior to terminal beta cell differentiation. Deciphering the precise mechanism will be important as it might unveil new pathways by which to manipulate beta cell mass that could be exploited as novel therapies for patients with diabetes. Springer-Verlag 2010-11-12 2011 /pmc/articles/PMC3017310/ /pubmed/21072627 http://dx.doi.org/10.1007/s00125-010-1963-x Text en © The Author(s) 2010 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Commentary
Matthews, L. C.
Hanley, N. A.
The stress of starvation: glucocorticoid restraint of beta cell development
title The stress of starvation: glucocorticoid restraint of beta cell development
title_full The stress of starvation: glucocorticoid restraint of beta cell development
title_fullStr The stress of starvation: glucocorticoid restraint of beta cell development
title_full_unstemmed The stress of starvation: glucocorticoid restraint of beta cell development
title_short The stress of starvation: glucocorticoid restraint of beta cell development
title_sort stress of starvation: glucocorticoid restraint of beta cell development
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3017310/
https://www.ncbi.nlm.nih.gov/pubmed/21072627
http://dx.doi.org/10.1007/s00125-010-1963-x
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