leptin and phorbol-12-13-didecanoate

The activation of PKC by the acute administration of the phorbol ester PMA (1 microM, 2h) to omental adipose tissue explants in vitro resulted in a marked (about 75%) and persistent (up to at least 96 h) inhibition of leptin secretion. This PKC-mediated inhibition was not observed after the administration of an inactive phorbol ester (phorbol 12,13-dicecanoate). The inhibition by PMA of leptin secretion was not restricted to the spontaneous secretion, but blocked also effectively the leptin response to a powerful stimulus, such as the glucocorticoid dexamethasone. As the PKC activity has been shown to be elevated during fasting, the negative relation here described between PKC activity and leptin secretion could be of physiological relevance.

Topics: Adipose Tissue; Aged; Dexamethasone; Enzyme Activation; Fasting; Female; Humans; In Vitro Techniques; Leptin; Male; Middle Aged; Phorbol Esters; Protein Kinase C; Proteins; Receptor, Insulin; Receptors, Leptin; Tetradecanoylphorbol Acetate