EFFECTS OF EPINEPHRINE ON LIPID-METABOLISM IN RESTING SKELETAL-MUSCLE

The effects of physiological (0, 0.1, 2.5, and 10 nM) and pharmacologi cal (200 nM) epinephrine concentrations on resting skeletal muscle lip id metabolism were investigated with the use of incubated rat epitroch learis (EPT), flexor digitorum brevis (FDB), and soleus (SOL) muscles. Muscles were chosen to reflect a range of oxidative capacities: SOL > EPT > FDB. The muscles were pulsed with [1-C-14]palmitate and chased with [9,10-H-3]palmitate. Incorporation and loss of the labeled palmit ate from the triacylglycerol pool (as well as mono- and diacylglycerol , phospholipid, and fatty acid pools) permitted the simultaneous estim ation of lipid hydrolysis and synthesis. Endogenous and exogenous fat oxidation was quantified by (CO2)-C-14 and (H2O)-H-3 production, respe ctively. Triacylglycerol breakdown was elevated above control at all e pinephrine concentrations in the oxidative SOL muscle, at 2.5 and 200 nM (at 10 nM, P = 0.066) in the FDB, and only at 200 nM epinephrine in the EPT. Epinephrine stimulated glycogen breakdown in the EPT at all concentrations but only at 10 and 200 nM in the FDB and had no effect in the SOL. We further characterized muscle lipid hydrolysis potential and measured total hormone-sensitive Lipase content by Western blotti ng (SOL > FDB > EPT). This study demonstrated that physiological level s of epinephrine cause measurable increases in triacylglycerol hydroly sis at rest in oxidative but not in glycolytic muscle, with no change in the rate of lipid synthesis or oxidation. Furthermore, epinephrine caused differential stimulation of carbohydrate and fat metabolism in glycolytic vs, oxidative muscle. Epinephrine preferentially stimulated glycogen breakdown over triacylglycerol hydrolysis in the glycolytic EPT muscle. Conversely, in the oxidative SOL muscle, epinephrine cause d an increase in endogenous lipid hydrolysis over glycogen breakdown.