Insulin-stimulated glucose oxidationwas enhanced by the addition of N6 (phenylisopropyladenosine(PIA), prostaglandin Et (PGE1) ornicotinic acid during a 1-h incubation of smallamounts (5–8 mg/ml) of rat fat cells. Basal lipolysiswas appreciable if low numbers of fat cells wereincubated per ml. Insulin inhibited basal lipolysisat 20 to 50 μU/ml and abolished lipolysis if 100μU/ml was present over a 1-h period. However PIA,PGE1 or nicotinic acid potentiated glucose oxidationdue to the 100 μU/ml dose of insulin indicating thatthese agents are not increasing glucose oxidationsolely as a result of an inhibition of lipolysis. PIA,PGE1 and nicotinic acid acted synergistically withinsulin in stimulating glucose oxidation and inhibitinglipolysis in the presence of norepinephrine.Insulin was unable to decrease basal cyclic AMPaccumulation or the increase in cyclic AMP seenwith norepinephrine and theophylline after varioustime periods (2 to 60 min) but PIA, PGE1 andnicotinic acid were able to inhibit cyclic AMPaccumulation at all times tested. (Endocrinology96: 1221, 1975)

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