CD24 is required for gene expression, but not glucose uptake, during adipogenesis in vitro

Adipose tissue dysfunction in obesity and lipodystrophy results in major health complications such as heart disease, stroke along with an increased risk for some cancers with obesity. CD24 is a cell surface receptor that has been shown to actively regulate lipid accumulation in adipocytes in vitro and in vivo. The goal of this project was to determine how CD24 regulates lipid accumulation. Glucose is a key substrate for de novo lipid synthesis but I found that knockdown of CD24 did not alter glucose uptake during adipogenesis. Instead, it caused the dysregulation of the expression of 134 genes as determined by DNA microarray analysis. I validated the changes to four of these genes during adipogenesis in 3T3-L1 pre-adipocytes in vitro. I also found that these genes were dysregulated when primary cells from the inguinal but not epididymal white adipose depot from CD24 knock-out mice were induced to undergo adipogenesis in vitro. Overall, the data presented here suggests that CD24 is necessary for select gene expression, but not glucose uptake, during adipogenesis in vitro. This new knowledge could help understand the regulation of lipid accumulation in adipocytes, to develop alternative treatment strategies for obesity and lipodystophy.