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An explanation of this in more laymans terms would be useful to me. Could one of you genius types please help me out? Thanks! ANGEL
copied from another board:
As for the evidence of permenant fat loss, I'm looking as we speak, and stumbled across this earlier:
Treatment of 3T3-L1 preadipocytes with arachidonic acid resulted in a dose-dependent inhibition of adipocyte differentiation. The cells failed to aculate fat droplets and did not express stearoyl-CoA desaturase 1 mRNA, a marker for late-stage differentiation. The inhibition of differentiation was reversed by the addition of cyclooxygenase inhibitors ibuprofen or indomethacin. Inhibitors of the lipoxygenase and cytochrome P-450 epoxygenase pathways were unable to reverse the effect of arachidonic acid. Dexamethasone, one of the adipogenic agents normally used to induce differentiation, could be replaced with cyclooxygenase inhibitors in the differentiation tail. This implicated dexamethasone as a modulator of prostaglandin synthesis in culture. Prostaglandins F[2?] (ED[50] = 0.4 nM), E[2], and D[2] prevented differentiation, each with a specific, dose-dependent affinity. Prostaglandin F[2?] was the most potent inhibitor of differentiation, suggesting that a prostanoid FP[2] receptor (FP receptor) mediates the prostaglandin action. Fluprostenol (ED[50] = 0.3 nM), a selective FP receptor agonist, prevented differentiation, confirming the involvement of an FP receptor in the inhibition of 3T3-L1 preadipocyte differentiation. Stimulation of the FP receptor for 1 h during the first day of differentiation was sufficient to cause substantial inhibition. Endogenous PGF[2?] production was lower in differentiating cells compared to unstimulated preadipocytes. These data suggest that PGF[2?] production by preadipocytes plays a role in maintaining the undifferentiated state.
copied from another board:
As for the evidence of permenant fat loss, I'm looking as we speak, and stumbled across this earlier:
Treatment of 3T3-L1 preadipocytes with arachidonic acid resulted in a dose-dependent inhibition of adipocyte differentiation. The cells failed to aculate fat droplets and did not express stearoyl-CoA desaturase 1 mRNA, a marker for late-stage differentiation. The inhibition of differentiation was reversed by the addition of cyclooxygenase inhibitors ibuprofen or indomethacin. Inhibitors of the lipoxygenase and cytochrome P-450 epoxygenase pathways were unable to reverse the effect of arachidonic acid. Dexamethasone, one of the adipogenic agents normally used to induce differentiation, could be replaced with cyclooxygenase inhibitors in the differentiation tail. This implicated dexamethasone as a modulator of prostaglandin synthesis in culture. Prostaglandins F[2?] (ED[50] = 0.4 nM), E[2], and D[2] prevented differentiation, each with a specific, dose-dependent affinity. Prostaglandin F[2?] was the most potent inhibitor of differentiation, suggesting that a prostanoid FP[2] receptor (FP receptor) mediates the prostaglandin action. Fluprostenol (ED[50] = 0.3 nM), a selective FP receptor agonist, prevented differentiation, confirming the involvement of an FP receptor in the inhibition of 3T3-L1 preadipocyte differentiation. Stimulation of the FP receptor for 1 h during the first day of differentiation was sufficient to cause substantial inhibition. Endogenous PGF[2?] production was lower in differentiating cells compared to unstimulated preadipocytes. These data suggest that PGF[2?] production by preadipocytes plays a role in maintaining the undifferentiated state.
