Exogenous XXXX stimulates adipogenesis of 3T3-L1 cells.

@entity897 @entity896 @entity9170 @entity19775 @entity16509 @entity1922 @entity21923 @entity619 @entity4301 @entity3240 @entity25525 @entity413 @entity13521
UNASSIGNED: We investigated the effects of exogenous @entity21923 (SP) on adipocyte differentiation, lipid accumulation, and the mRNA expression levels of adipogenesis-related genes in 3T3-L1 pre-adipocytes. Differentiation of pre-adipocytes was induced by @entity13521 ( @entity1922 : @entity1922 , @entity619 : @entity9170 , and insulin), in the presence or absence of SP. Adipogenesis was stimulated by SP in a concentration-dependent manner. SP also induced the expression of genes encoding @entity25525 , @entity3240 , and adiponectin, but had no effect on cell proliferation. Exogenous @entity413 did not promote adipogenesis or lipid accumulation. @entity897 inhibited adipogenesis initiated by @entity13521 , but failed to influence the effects of SP on adipogenesis, whereas @entity896 inhibited adipogenesis regardless of whether SP was present. The pro-adipogenic properties of SP were limited to the early events of adipogenesis. To determine whether SP mimics the adipogenic action of @entity619 or insulin, we examined the effects of SP on adipogenesis with combinations of @entity1922 , @entity9170 , and insulin. SP did not improve incomplete lipid accumulation observed in cells grown under @entity1922 -, @entity9170 -, or insulin-free conditions. Insulin-stimulated ERK1/2 phosphorylation was diminished by SP, while phosphorylation of Akt was increased, correlating with increased @entity413 uptake in response to insulin. We also observed that SP stimulated immediate early expression of @entity19775 and @entity16509  . The PPARy antagonist @entity4301 inhibited adipogenesis. Our findings highlight the adipogenic function of exogenous SP by stimulating early events of adipogenesis.
