Journal
DEVELOPMENTAL CELL
Volume 32, Issue 5, Pages 535-545Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2015.01.002
Keywords
-
Categories
Funding
- beta-cell Biology Consortium
- JDRF
- ERC
- EU/FP7 (BetaCellTherapy) [241883]
- Helmsley Charitable trust
- DON foundation
- BIRAX
- ISF
- I-CORE Program of The Israel Science Foundation [41.11]
- USAID's American Schools and Hospitals Abroad Program for the upgrading of the Hebrew University Medical School Flow Cytometry laboratory
- Novo Nordisk
Ask authors/readers for more resources
Because tissue regeneration deteriorates with age, it is generally assumed that the younger the animal, the better it compensates for tissue damage. We have examined the effect of young age on compensatory proliferation of pancreatic beta cells in vivo. Surprisingly, beta cells in suckling mice fail to enter the cell division cycle in response to a diabetogenic injury or increased glycolysis. The potential of beta cells for compensatory proliferation is acquired following premature weaning to normal chow, but not to a diet mimicking maternal milk. In addition, weaning coincides with enhanced glucose-stimulated oxidative phosphorylation and insulin secretion from islets. Transcriptome analysis reveals that weaning increases the expression of genes involved in replication licensing, suggesting a mechanism for increased responsiveness to the mitogenic activity of high glucose. We propose that weaning triggers a discrete maturation step of beta cells, elevating both the mitogenic and secretory response to glucose.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available