Journal
CURRENT OPINION IN CELL BIOLOGY
Volume 19, Issue 6, Pages 634-645Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.ceb.2007.09.015
Keywords
-
Categories
Funding
- NIDDK NIH HHS [R01 DK068763-02, R01 DK068763, R01 DK-068763] Funding Source: Medline
Ask authors/readers for more resources
The elaboration of the pancreas from epithelia[ buds to the intricate organ requires complex patterning information that controls fundamental cellular processes such as differentiation and proliferation of pancreatic progenitor cells. During pancreatic organogenesis, endocrine cells are generated from a population of pancreatic progenitor cells. The progenitor cells during the early development simultaneously receive multiple signals, some mitogenic and some inducing differentiation. These extrinsic signals are interpreted through an intrinsic mechanism that either commits the progenitor cell to the mitotic cell cycle or leads to exit from the cell cycle in order to differentiate. The endocrine cells that differentiate from progenitor cells are postmitotic, and direct lineage tracing analyses indicate that a population of progenitor cells persists throughout embryogenesis to allow the differentiation of new endocrine cells. At the end of embryogenesis an early postnatal period is characterized by high rates of beta cell proliferation leading to massive increases in beta cell mass. The beta cell mass expansion considerably slows down in adult animals, though variations in insulin demand due to physiological and pathological states such as pregnancy and obesity can lead to adaptive changes in the beta cells that include hyperplasia, hypertrophy, and increased insulin synthesis and secretion. Deciphering the mechanisms that regulate the plasticity of beta cell mass can be an important step in developing effective strategies to treat diabetes.
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