• S Klein, E J Peters, O B Holland, and R R Wolfe.
• Department of Internal Medicine, University of Texas Medical Branch, Galveston.
• Am. J. Physiol. 1989 Jul 1; 257 (1 Pt 1): E65-73.

AbstractStable isotope tracers and indirect calorimetry were used to evaluate the importance of beta-adrenergic stimulation of lipolysis and triglyceride-fatty acid cycling during fasting in healthy human volunteers. Each subject was studied after 12 and 84 h of fasting both with and without propranolol infusion (protocol 1) and when oral propranolol treatment was given throughout fasting (protocol 2). In protocol 1, the rates of appearance of glycerol and palmitic acid increased from 3.04 +/- 0.19 and 1.78 +/- 0.17 mumol.kg lean body mass-1.min-1, respectively, after 12 h of fasting to 5.28 +/- 0.31 and 3.47 +/- 0.15 mumol.kg lean body mass-1.min-1, respectively, after 84 h of fasting (P less than 0.005). The rate of triglyceride-fatty acid cycling increased from 97 +/- 8 to 169 +/- 5 mumol/min (P less than 0.005). Intravenous propranolol infusion decreased the rate of lipolysis after both 12 and 84 h of fasting, but the magnitude of the antilipolytic effect was much greater after 84 h (P less than 0.005). In protocol 2, the rate of lipolysis and triglyceride-fatty acid cycling was still increased by fasting despite beta-adrenergic blockade with oral propranolol. This study demonstrates that beta-adrenergic stimulation contributes to the mobilization of fat during fasting. However, other mechanism(s) can increase lipolysis and triglyceride-fatty acid cycling when beta-adrenergic receptors are continuously blocked.

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