Abstract

Prolonged treatment of adipocytes with certain inhibitors of lipolysis, including N 6-phenylisopropyl adenosine (PIA) and prostaglandin E 1 (PGE 1) leads to down-regulation of G i. Prolonged treatment with PIA increases the rate of lipolysis, and we have reported that tumor necrosis factor-α (TNFα) stimulates lipolysis by down-regulating G i. To determine the relationship between G i concentration and lipolysis, we have investigated the effect of two other acute inhibitors of lipolysis; PGE 1, which down-regulates G i, and nicotinic acid (NA), which does not down-regulate G i. Rat adipocytes were incubated with PIA (300 nM), PGE 1 (3 μM) or nicotinic acid (1 mM) for 24 h. The rate of lipolysis (glycerol release) was increased approximately 2 to 3-fold in PIA-treated cells, and in PGE 1-treated cells. Conversely, the rate of lipolysis was not altered by the prolonged nicotinic acid treatment. These findings support the hypothesis that the rate of lipolysis in adipocytes is determined, at least partly, by the cellular concentration of G i proteins.

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