Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 223-226 |
| Number of pages | 4 |
| Journal | Diabetologia |
| Volume | 54 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Feb 2011 |
Bibliographical note
Funding Information:Acknowledgements The authors receive support from the Manchester National Institute for Health Research Biomedical Research Centre. L. C. Matthews is a University of Manchester Stepping Stones Fellow. N. A. Hanley is a Wellcome Trust Senior Fellow in Clinical Science in addition to receiving funding from the Biotechnology and Biological Sciences Research Council, the Engineering and Physical Sciences Research Council, and Stem Cells for Safer Medicine.
Keywords
- Beta cell
- Corticosterone
- Cortisol
- Development
- Glucocorticoid
- Glucocorticoid receptor
- Human
- Insulin
- Mouse
- Neurogenin 3
- Pancreas
- Under-nutrition
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism
