|Start Date / Time||April 23, 2014 at 9:00 AM|
|End Date / Time||April 23, 2014 at 10:00 AM|
|Location||512 Light Hall|
|Presenter Name||Maria Golson (Gannon)|
|Presentation Title||Using activated FoxM1 to enhance beta cell function and proliferation|
|Status||This meeting has already occurred|
FoxM1 is a transcription factor required for b-cell replication during normal postnatal growth, during gestation, and after partial pancreatectomy. Yet, transgenic overexpression of FoxM1 is not sufficient to augment b-cell mass, even after injury, possibly due to posttranslational regulation of FoxM1. To partially bypass this regulation, we derived a transgenic mouse line expressing an inducible, activated form of FoxM1 in b-cells (b-FoxM1* mice). While activated FoxM1 did not alter b-cell mass in two-month old mice, two weeks of expression in four-, eight- and twelve-month old mice effected increased b-cell mass, demonstrating rejuvenation of replicative potential. Unexpectedly, b-FoxM1* mice displayed enhanced insulin secretion and improved glucose homeostasis at two months, before any b-cell mass increase.