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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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Formato: | Texto |
Lenguaje: | English |
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Springer-Verlag
2010
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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. |
format | Text |
id | pubmed-3017310 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Springer-Verlag |
record_format | MEDLINE/PubMed |
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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