| Abstract
| - We have previously reported that grape seed procyanidins stimulate long-term lipolysis on 3T3-L1fully differentiated adipocytes. To unravel the molecular mechanism by which procyanidins exert thiseffect, we checked the involvement of two main cellular targets in adipose cells: protein kinase A(PKA) and peroxisome proliferator-activated receptor-γ (PPAR-γ). Procyanidin treatment increasedintracellular cAMP levels in 3T3-L1 adipocytes, and their lipolytic effect was inhibited by simultaneoustreatment with H89, a PKA specific inhibitor. BRL49653, a very highly specific ligand of PPAR-γ,totally abolished the lipolytic effect of procyanidins. Simultaneous to this long-term lipolytic effect,the mRNA levels of some differentiation adipocyte markers decreased, although there were nochanges in the triglyceride content of the cells. BRL49653 did not antagonize the decrements ofdifferentiation markers. These results support a mediation of PPAR-γ and PKA on the lipolytic effectsof procyanidins on 3T3-L1 adipocytes. Keywords: Procyanidin; lipolysis; protein kinase A; PPAR-γ2; 3T3-L1
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