CD36 may regulate glycolytic and steroidogenic processes but not the fatty acid uptake in bovine granulosa cells

Postpartum metabolic stress increases non-esterified fatty acid (NEFA) concentration in follicular fluid, thereby impairing oocyte and granulosa cell (GC) function. CD36, a multifunctional scavenger receptor, is involved in the uptake of NEFAs in various cell types. This study examines lipid droplet (LD) accumulation and CD36 expression in GCs treated with oleate (OA), palmitate (PA), stearate (SA), and their combination. We also explored the role of CD36 in lipid uptake, glucose metabolism, and steroidogenesis in GCs. Flow cytometry analysis revealed that SA, OA, and the combined NEFA treatments resulted in significant LD accumulation, while PA had a minimal effect. Interestingly, CD36 expression mirrored the levels of LD accumulation in all treatments. However, SLC27A1, another highly expressed NEFA transporter, was upregulated by SA but was unchanged by PA and OA treatments. Combination of OA, PA, and SA has increased both CD36 and SLC27A1 expression. OA treatment induced a dose-dependent increase in LD accumulation and CD36 expression. However, CD36 knockdown did not affect either LD accumulation or triglyceride levels, indicating that CD36 is not essential for NEFA uptake, despite its increased expression. Previously, we showed that OA enhances glycolysis in GCs; here, we found that CD36 is involved in glucose metabolism as its silencing significantly reduced the extracellular acidification rate and mitochondrial membrane potential in GCs. Furthermore, CD36 knockdown significantly reduced progesterone production. These findings suggest that while CD36 is dispensable for NEFA uptake, it may play a regulatory role in maintaining glycolytic activity, mitochondrial function, and steroidogenesis in GCs under elevated NEFA levels.