Journal
AGING-US
Volume 2, Issue 10, Pages 650-658Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/aging.100200
Keywords
Telomere; telomerase; senescence; diabetes mellitus; glucose intolerance; Insulin secretion; beta-cell
Categories
Funding
- German Ministry for Education
- Bundesministerium fur Bildung und Forschung - BMBF [0315581[A-D]]
Ask authors/readers for more resources
Reduced telomere length and impaired telomerase activity have been linked to several diseases associated with senescence and aging. However, a causal link to metabolic disorders and in particular diabetes mellitus is pending. We here show that young adult mice which are deficient for the Terc subunit of telomerase exhibit impaired glucose tolerance. This is caused by impaired glucose-stimulated insulin secretion (GSIS) from pancreatic islets, while body fat content, energy expenditure and insulin sensitivity were found to be unaltered. The impaired secretion capacity for insulin is due to reduced islet size which is linked to an impaired replication capacity of insulin-producing beta-cells in Terc-deficient mice. Taken together, telomerase deficiency and hence short telomeres impair replicative capacity of pancreatic beta-cells to cause impaired insulin secretion and glucose intolerance, mechanistically defining diabetes mellitus as an aging-associated disorder.
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