|Start Date / Time||November 19, 2014 at 9:00 AM|
|End Date / Time||November 19, 2014 at 9:55 AM|
|Location||512 Light Hall|
|Presenter Name||Benjamin Glaser, MD, Hadassah-Hebrew Univ Med Ctr|
|Presentation Title||Glycolysis Control of Beta-cell Fate|
|Status||This meeting has already occurred|
Pancreatic beta-cell plasticity, defined as its ability to self-replicate, de-differentiate and trans-differentiate, has recently become the subject of extensive study. Beta-cell glycolytic flux, and thus demand for insulin secretion (work-load), appears to be the major regulator controlling entry into the cell cycle. However, increased glycolytic flux also has a toxic effect, modulated by expression of p53, evidence suggesting DNA damage as well as evidence of de-differentiation and even trans-differentiation to other endocrine cell types. GLP1 agonists may be able to prevent, at least partially, these toxic effects.