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.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Burkart, Alison Marie

Publisher

• Worcester Polytechnic Institute

Identifier

• 02B030M

Advisor

• Adams, David S.

Year

• 2002

Date created

• 2002-01-01

Resource type

• Major Qualifying Project

Major

• Biology & Biotechnology

Rights statement

• In Copyright