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Systemic Regulation of the Age-Related Decline of Pancreatic β-Cell Replication
The frequency of pancreatic β-cell replication declines dramatically with age, potentially contributing to the increased risk of type 2 diabetes in old age. Previous studies have shown the involvement of cell-autonomous factors in this phenomenon, particularly the decline of polycomb genes and accum...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Diabetes Association
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3717843/ https://www.ncbi.nlm.nih.gov/pubmed/23630298 http://dx.doi.org/10.2337/db13-0160 |
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author | Salpeter, Seth J. Khalaileh, Abed Weinberg-Corem, Noa Ziv, Oren Glaser, Benjamin Dor, Yuval |
author_facet | Salpeter, Seth J. Khalaileh, Abed Weinberg-Corem, Noa Ziv, Oren Glaser, Benjamin Dor, Yuval |
author_sort | Salpeter, Seth J. |
collection | PubMed |
description | The frequency of pancreatic β-cell replication declines dramatically with age, potentially contributing to the increased risk of type 2 diabetes in old age. Previous studies have shown the involvement of cell-autonomous factors in this phenomenon, particularly the decline of polycomb genes and accumulation of p16/INK4A. Here, we demonstrate that a systemic factor found in the circulation of young mice is able to increase the proliferation rate of old pancreatic β-cells. Old mice parabiosed to young mice have increased β-cell replication compared with unjoined old mice or old mice parabiosed to old mice. In addition, we demonstrate that old β-cells transplanted into young recipients have increased replication rate compared with cells transplanted into old recipients; conversely, young β-cells transplanted into old mice decrease their replication rate compared with young cells transplanted into young recipients. The expression of p16/INK4A mRNA did not change in heterochronic parabiosis, suggesting the involvement of other pathways. We conclude that systemic factors contribute to the replicative decline of old pancreatic β-cells. |
format | Online Article Text |
id | pubmed-3717843 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | American Diabetes Association |
record_format | MEDLINE/PubMed |
spelling | pubmed-37178432014-08-01 Systemic Regulation of the Age-Related Decline of Pancreatic β-Cell Replication Salpeter, Seth J. Khalaileh, Abed Weinberg-Corem, Noa Ziv, Oren Glaser, Benjamin Dor, Yuval Diabetes Original Research The frequency of pancreatic β-cell replication declines dramatically with age, potentially contributing to the increased risk of type 2 diabetes in old age. Previous studies have shown the involvement of cell-autonomous factors in this phenomenon, particularly the decline of polycomb genes and accumulation of p16/INK4A. Here, we demonstrate that a systemic factor found in the circulation of young mice is able to increase the proliferation rate of old pancreatic β-cells. Old mice parabiosed to young mice have increased β-cell replication compared with unjoined old mice or old mice parabiosed to old mice. In addition, we demonstrate that old β-cells transplanted into young recipients have increased replication rate compared with cells transplanted into old recipients; conversely, young β-cells transplanted into old mice decrease their replication rate compared with young cells transplanted into young recipients. The expression of p16/INK4A mRNA did not change in heterochronic parabiosis, suggesting the involvement of other pathways. We conclude that systemic factors contribute to the replicative decline of old pancreatic β-cells. American Diabetes Association 2013-08 2013-07-17 /pmc/articles/PMC3717843/ /pubmed/23630298 http://dx.doi.org/10.2337/db13-0160 Text en © 2013 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details. |
spellingShingle | Original Research Salpeter, Seth J. Khalaileh, Abed Weinberg-Corem, Noa Ziv, Oren Glaser, Benjamin Dor, Yuval Systemic Regulation of the Age-Related Decline of Pancreatic β-Cell Replication |
title | Systemic Regulation of the Age-Related Decline of Pancreatic β-Cell Replication |
title_full | Systemic Regulation of the Age-Related Decline of Pancreatic β-Cell Replication |
title_fullStr | Systemic Regulation of the Age-Related Decline of Pancreatic β-Cell Replication |
title_full_unstemmed | Systemic Regulation of the Age-Related Decline of Pancreatic β-Cell Replication |
title_short | Systemic Regulation of the Age-Related Decline of Pancreatic β-Cell Replication |
title_sort | systemic regulation of the age-related decline of pancreatic β-cell replication |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3717843/ https://www.ncbi.nlm.nih.gov/pubmed/23630298 http://dx.doi.org/10.2337/db13-0160 |
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