An anti-leptin receptor polyclonal antibody (receptor antibody), as well as leptin, stimulated the release of free fatty acids from isolated mouse fat pads in a timedependent manner. Following a 90-min incubation, maximal lipolysis was observed at 6 g/ml receptor antibody and 0.1 nM leptin. The receptor antibody did not show any additive effect to the stimulation of lipolysis induced by leptin, suggesting that they exert their actions through a similar mechanism involving the leptin receptor. N -[2-( pbromocinnamylamino) ethyl]-5-isoquinolinesulfonamide (H-89), quin 2-AM, N -(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), and neomycin sulfate (neomycin) all potently inhibited the stimulation of lipolysis by the receptor antibody and leptin. Short-term incubation of the fat pads with the receptor antibody or leptin showed a transient increase in the cellular content of cAMP and myo -inositol 1,4,5-trisphosphate (IP 3 ) in similar concentrations to the free fatty acid release. Quin 2-AM and W-7 also inhibited the increase in cAMP content, suggesting that a Ca 2 ϩ /calmodulindependent process may be involved in a part of the mechanism in which the receptor antibody and leptin exert their effects. The increase in cellular IP 3 content via phosphoinositide-specific phospholipase C (PLC) sensitive to neomycin appears to be a primary step to initiate intracellular events. Both the receptor antibody and leptin may stimulate the lipolysis through mechanisms involving a transient increase in the cellular IP 3 content followed by cAMP production, which leads to the activation of cAMP-dependent protein kinase. -Kawaji, N., A. Yoshida, T. Motoyashiki, T. Morita, and H. Ueki. Anti-leptin receptor antibody mimics the stimulation of lipolysis induced by leptin in isolated mouse fat pads.
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