Elevation of plasma epinephrine concentrations inhibits proteolysis and leucine oxidation in man via β-adrenergic mechanisms

Abstract

The role of elevated plasma epinephrine concentrations in the regulation of plasma leucine kinetics and the contribution of β-receptors were assessed in man. Epinephrine (50 ng/kg per min) was infused either alone or combined with propranolol (β-blockade) into groups of six subjects fasted overnight; leucine flux, oxidation, and net plasma leucine forearm balance were determined during 180 min. Constant plasma insulin and glucagon concentrations wee maintained in all studies by infusion somatostatin combined with insulin and glucagon replacements. Plasma leucine concentrations decreased from baseline during epinephrine infusion by 27 ± 5 μmol/liter (P < 0.02) due to a 22 ± 6% decrease in leucine flux (P < 0.05 vs. controls receiving saline) and to an increase in the metabolic clearance rate of leucine (P < 0.02). Leucine oxidation decreased by 36 ± 8% (P < 0.01 vs. controls). β Blockade abolished the effect of epinephrine on leucine flux and oxidation. Net forearm release of leucine increased during epinephrine (P < 0.01), suggesting increased muscle proteolysis; the fall of total body leucine flux was therefore due to diminished proteolysis in nonmuscle tissues, such as splanchnic organs. Non-oxidative leucine disappearance as a parameter of protein synthesis was not significantly influenced by epinephrine. Plasma glucose and FFA concentrations increased via β-adrenergic mechanisms (P < 0.001). The results suggest that elevation of plasma epinephrine concentrations similar to those observed in severe stress results in redistribution of body proteins and exerts a whole body protein-sparing effect; this may counteract catabolic effects of other hormones during severe stress.