Faculty Advisor

Adams, David S.

Abstract

Rosiglitazone is a current Type 2 diabetes drug. Two theories about rosiglitazone's therapeutic mechanism are: new insulin responsive adipocytes form, or that pre-existing insulin-resistant adipocytes improve. We hypothesize that rosiglitazone alone is unable to generate new, insulin-responsive adipocytes. Using 3T3-L1 cells as a model, different differentiation conditions were tested in order to determine the effect of rosiglitazone on 3T3-L1 differentiation. The physical state of the cells was compared by immunofluorescence of key marker proteins. Biochemical studies were used to monitor differences in protein regulation. Mitochondrial biogenesis was also examined. The results indicated that rosiglitazone has no substantial effect on adipogenesis.

Publisher

Worcester Polytechnic Institute

Date Accepted

January 2002

Major

Biology and Biotechnology

Project Type

Major Qualifying Project

Accessibility

Restricted-WPI community only

Advisor Department

Biology and Biotechnology

Share

COinS