Acute, oral ethanol administration suppresses episodic growth hormone secretion in the male rat.

The effect of single dose ethanol administration on GH secretion was studied in young adult male rats bearing indwelling gastric and right-atrial cannulas. Rats (nonfasted) received saline or ethanol (1, 2, 3, or 4 g/kg) via gastric cannula 2h before the onset of the daily dark period; blood was sampled every 15 min for 5 h. Each rat served as its own control, receiving saline and one ethanol dose separated by 2-3 days. Plasma samples were assayed for ethanol, GH, and testosterone. On saline days, all rats showed typical, episodic peaks of GH in plasma. This pattern was unaffected by ethanol at 1 g/kg (peak plasma ethanol approximately 65 mg/100 ml). Ethanol at 2 g/kg caused a rapid, marked, but not total suppression of plasma GH levels (peak plasma ethanol approximately 140 mg/100 ml), whereas at doses of 3 or 4 g/kg ethanol, a total suppression of GH secretion occurred (peak plasma ethanol approximately 190 and 240 mg/100 ml, respectively). Plasma testosterone levels showed a similar dose-sensitivity to ethanol. The threshold for GH suppression appears to be around 100 mg/100 ml plasma ethanol and is sustained throughout the time period examined, despite falling ethanol levels.

Diet-induced changes in serum cholesterol concentrations do not alter tryptophan hydroxylation rate or serotonin concentrations in gerbil brain.

The relationship between serum cholesterol concentrations and serotonin synthesis rate in brain was examined in Mongolian gerbils chronically fed diets containing 20% fat (safflower oil, beef tallow or butterfat) with or without added cholesterol (0.5%, dry weight). After 22 days on these diets, circulating cholesterol concentrations ranged between approximately 1.5 and approximately 20 mumol/ml. Despite this enormous range, in vivo tryptophan hydroxylation rate, and serotonin and 5-hydroxyindoleacetic acid concentrations in cerebral cortex, hypothalamus and brainstem did not differ significantly among the diet groups. Tryptophan concentrations in serum and brain were also unaffected. These results do not support the hypothesis that the link between depression, suicide and violent deaths and below-normal or reduced serum cholesterol concentrations in humans involves an alteration in serotonin synthesis and/or release by brain neurons.