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Catecholamines (CA) inhibit leptin secretion. Alcohol appears to have a similar effect. The mechanism underlying the inhibitory effect of alcohol is unknown, but CA may play a role as mediators. This hypothesis has never been tested. We decided to do so in the present investigation.


Seven healthy subjects participated in two experiments (A and B), performed in random order, 1 week apart. In experiment A, three identical doses of ethanol (0.45 g/kg b.w.) were ingested at regular intervals between 09:00 and 12:00 hours. The alcohol doses were given against a background of oral placebo administered at 08:00 and 12:00 hours. In experiment B, identical doses of alcohol were ingested against a background of oral propranolol (40 mg at 08:00 and 20 mg at 12:00 hours). Pulse rates, and serum levels of ethanol, insulin, IGF-1 and leptin, were determined at regular intervals throughout the experiments. Urinary CA excretion was also determined.


Propranolol (experiment B) decreased the pulse rate significantly, compared with placebo (experiment A), but did not change the urinary excretion of adrenaline nor noradrenaline. Alcohol ingestion raised the serum ethanol levels similarly in the two experiments but did not affect the insulin or IGF-1 levels. The serum leptin levels declined similarly in the two experiments, as evidenced by the percentage serum leptin decline from baseline, which was 28.6 ± 5.4% in experiment A and 29.0 ± 2.9% in experiment B.


The declining serum leptin concentration after acute ingestion of alcohol does neither appear to be CA-mediated nor to be caused by changed secretion of insulin or IGF-1. A direct inhibitory effect of alcohol on the adipocytes is possible, but increased disposal of leptin via hepatic metabolism or renal excretion could also contribute.

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