Abstract
Chronically elevated levels of glucose impair pancreatic beta-cell function while inducing beta-cell proliferation. MicroRNA-29a (miR-29a) levels are increased in several tissues in diabetic animals and mediate decreased insulin-stimulated glucose-transport of adipocytes. The aim was to investigate the impact of glucose on miR-29a levels in INS-1E beta-cells and in human islets of Langerhans and furthermore to evaluate the impact of miR-29a on beta-cell function and proliferation. Increased glucose levels up-regulated miR-29a in beta-cells and human and rat islets of Langerhans. Glucose-stimulated insulin-secretion (GSIS) of INS-1E beta-cells was decreased by forced expression of miR-29a, while depletion of endogenous miR-29a improved GSIS. Over-expression of miR-29a increased INS-1E proliferation. Thus, miR-29a up-regulation is involved in glucose-induced proliferation of beta-cells. Furthermore, as depletion of miR-29a improves beta-cell function, miR-29a is a mediator of glucose-induced beta-cell dysfunction. Glucose-induced up-regulation of miR-29a in beta-cells could be implicated in progression from impaired glucose tolerance to type 2 diabetes.
| Original language | English |
|---|---|
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 426 |
| Issue number | 2 |
| Pages (from-to) | 266-72 |
| Number of pages | 7 |
| ISSN | 0006-291X |
| DOIs | |
| Publication status | Published - 21 Sept 2012 |
Keywords
- Animals
- Cell Line
- Cell Proliferation
- Cell Size
- Glucose
- Glucose Intolerance
- Humans
- Insulin
- Insulin-Secreting Cells
- MicroRNAs
- Rats
- Up-Regulation
