| Summary: | Fat cells isolated from rat epididymal adipose tissue were incubated with albumin-bound [14C]palmitate. Incorporation of 14C into 14CO2 and glycerides was measured. Some evidence is presented to suggest that the exogenous palmitate pool is in isotopic equilibrium with intracellular precursors for these metabolic processes. Precautions were taken to minimize dilution of the exogenous palmitate pool by fatty acids released from the cells. 14CO2 production from [1-14C]palmitate was 3 times that from [16-14C]palmitate. Octanoate increased this differential oxidation of palmitate carbons and also inhibited palmitate oxidation without similarly affecting esterification. Glucose increases palmitate esterification in cells from fed or starved rats. Insulin potentiated this effect of glucose. Glucose influenced palmitate oxidation in a more complex manner, dependent upon the glucose concentration. Both the observation that esterification constitutes 99% of the metabolic flux of fatty acid and the manner in which glucose, insulin, or starvation influence palmitate esterification and oxidation suggested that factors controlling esterification may alter oxidation as a secondary effect, but not vice versa. It is suggested that oxidation and esterification compete for a single intracellular precursor, possibly extramitochondrial long chain fatty acyl CoA.
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