AI Article Synopsis
- The study investigates how anti-adipogenic factors like platelet-derived growth factor (PDGF) inhibit the differentiation of preadipocytes compared to pro-adipogenic factors like insulin.
- PDGF was shown to activate IKKbeta through phosphorylation, which is dependent on the PI 3-kinase/AKT pathway, while insulin did not trigger this response.
- The inhibition of adipocyte differentiation by PDGF led to significant reductions in triacylglycerol accumulation and fatty acid synthase expression, effects that were negated when IKKbeta activity was blocked.
Article Abstract
To clarify how anti-adipogenic factors act on preadipocytes to inhibit their differentiation, we compared preadipocyte signaling responses generated by platelet-derived growth factor (PDGF; anti-adipogenic) versus insulin (pro-adipogenic). PDGF, but not insulin, stimulated the phosphorylation of inhibitor of kappaB kinase beta (IKKbeta) in a time-dependent manner. This PDGF-dependent phosphorylation event was inhibited by 60% (P<0.05) when the cells were pretreated with wortmannin, indicating a requirement for the phosphatidylinositol (PI) 3-kinase/AKT pathway. IKKbeta phosphorylation by PDGF was neither accompanied by IkappaBalpha degradation nor NF-kappaB activation. PDGF inhibited human adipocyte differentiation, assessed by triacylglycerol accumulation (75% reduction; P<0.01) and by fatty acid synthase protein expression (60% reduction; P<0.05); these responses were no longer apparent in the presence of sc-514, a selective inhibitor of IKKbeta. Our data describe a novel PDGF response in human preadipocytes that involves the pro-inflammatory kinase IKKbeta and demonstrate that it is required for the inhibition of adipogenesis.
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| http://dx.doi.org/10.1677/JOE-08-0411 | DOI Listing |
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