β-cell proliferation is the major source of new pancreatic β cells
Author:
Publisher
Springer Science and Business Media LLC
Subject
Endocrinology,Endocrinology, Diabetes and Metabolism
Link
http://www.nature.com/articles/ncpendmet0187.pdf
Reference10 articles.
1. Kulkarni RN et al. (2004) PDX-1 haploinsufficiency limits the compensatory islet hyperplasia that occurs in response to insulin resistance. J Clin Invest 114: 828–836
2. Dor Y et al. (2004) Adult pancreatic beta-cells are formed by self-duplication rather than stem-cell differentiation. Nature 429: 41–46
3. Uchida T et al. (2005) Deletion of Cdkn1b ameliorates hyperglycemia by maintaining compensatory hyperinsulinemia in diabetic mice. Nat Med 11: 175–182
4. Rane SG et al. (1999) Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia. Nat Genet 22: 44–52
5. Martin J et al. (2003) Genetic rescue of Cdk4 null mice restores pancreatic beta-cell proliferation but not homeostatic cell number. Oncogene 22: 5261–5269
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