The mechanism of inhibition of 3T3-L1 preadipocyte differentiation by prostaglandin F2alpha.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

We have shown previously that treatment of 3T3-L1 preadipocytes with prostaglandin F2alpha (PGF2alpha) and fluprostenol, a prostanoid FP2 receptor (FP receptor) agonist, inhibited adipocyte differentiation. In this study, we demonstrate that the inhibition by PGF2alpha is controlled by concentrations of PGF2alpha rather than regulation of FP receptor levels or binding. Membranes prepared from either 3T3-L1 preadipocytes or adipocytes exhibited specific binding for PGF2alpha, suggesting that FP receptors are present throughout differentiation. Endogenous PGF2alpha production in 3T3-L1s was lower in differentiating cells compared with uninduced preadipocytes, providing further evidence that regulation occurs at the level of ligand concentration. Stimulation of the FP receptor causes a transient intracellular calcium increase, an activation of a calcium/calmodulin-dependent protein kinase (CaMK), and an increase in DNA synthesis, associated with the inhibition of differentiation. Calcium mobilizing agents, A23187 and thapsigargin, mimic the FP receptor-induced inhibition of differentiation, suggesting a role for calcium. KN-62, a CaMK inhibitor, reversed the inhibition of differentiation when added to differentiating cells with fluprostenol, suggesting a critical role for a CaMK in the inhibition. The activation of CaMK was responsible for an increase in DNA content and thymidine

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.