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**phoenix1927** · 05-03-2010, 01:35 PM

J Clin Endocrinol Metab 1996 Jul;81(7):2627-32
Ethanol decreases nocturnal plasma levels of thyrotropin and growth hormone but not those of thyroid hormones or prolactin in man.
Ekman AC, Vakkuri O, Ekman M, Leppaluoto J, Ruokonen A, Knip M.

Previous studies on the effects of ethanol on circulating pituitary hormones have been carried out mostly during daytime when the secretion of these hormones is generally at a nadir. Therefore, we studied the effects of ethanol on the nocturnal secretion of GH, PRL, TSH, and thyroid hormones (protocol I, nine healthy subjects, five women) and on the TSH and PRL responses to synthetic TRH (protocol II, healthy subjects, four women). Ethanol was given in doses of 0, 0.5 or 1.0 g/kg of BW(protocol I) and 0 or 1.0 g/kg (protocol II) and ingested po at 1900-1945 h. In protocol I, plasma GH rose from 0.6 +/- 0.2 microgram/L (mean +/- SE) at 2200 h to 25.0 +/- 4.3 micrograms/L at 0100 h in control subjects and was almost completely inhibited at 4.5 +/- 1.7 micrograms/L at 0100 h in subjects receiving 1.0 g/kg ethanol (P < 0.01). In subjects receiving 0.5 g/kg ethanol, the inhibition was also significant (P < 0.01), plasma GH being 8.2 +/- 2.5 micrograms/L at 0100 h. Plasma GHRH was measured after solid phase separation in RIA, but it did not show any ethanol-related changes. Plasma PRL exhibited a clear diurnal rhythm in control subjects and rose from 77 +/- 16 at 1800 h to 248 +/- 62 micrograms/L at 0700 h (P < 0.01). The plasma PRL profile was not affected by ethanol. Plasma TSH was 1.4 +/- 0.2 mU/L at 1800-2200 h and rose to 2.3-2.4 mU/L for 0100-0700 h (P < 0.001) in the control subjects. Ethanol 1.0 g/kg suppressed plasma TSH to 1.4 +/- 0.2 mU/L (P < 0.05 at 0100 h and P < 0.01 at 0200 h). According to the area under the curve analyses, the suppression in the nocturnal TSH was 32% in the 0.5 g/kg group and 45% in the 1.0 g/kg group (P < 0.05 for both cases). Circulating free or total T3 and T4 did not show any statistically significant changes that could explain the ethanol-induced inhibition in the nocturnal TSH peak. In protocol II, synthetic TRH (1 microgram/kg BW) was given intravenously, and blood samples were collected before, at 20 and 60 min. TRH significantly stimulated plasma TSH and PRL, but ethanol (1.0 g/kg BW) had no effect on these responses. In conclusion, small amounts of ethanol have unexpectedly great effects on nocturnal surges of TSH, and especially on those of GH, that are apparently mediated by suprapituitary mechanisms. On the other hand, ethanol did not affect the nocturnal PRL surge. These inhibitory effects of ethanol may have unfavorable effects on growth and metabolism in adolescent drinkers.

**phoenix1927** · 05-03-2010, 01:37 PM

J Appl Physiol 2002 Mar;92(3):1176-82
Acute ethanol increases angiogenic growth factor gene expression in rat skeletal muscle.

Gavin TP, Wagner PD.

Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623, USA.

Moderate ethanol consumption demonstrates a protective effect against cardiovascular disease and improves insulin sensitivity, possibly through angiogenesis. We investigated whether 1) ethanol would increase skeletal muscle growth factor gene expression and 2) the effects of ethanol on skeletal muscle growth factor gene expression were independent of exercise-induced growth factor gene expression. Female Wistar rats were used. Four groups (saline + rest; saline + exercise; 17 mmol/kg ethanol + rest; and 17 mmol/kg ethanol + exercise) were used to measure the growth factor response to acute exercise and ethanol administration. Vascular endothelial growth factor (VEGF), transforming growth factor-beta(1) (TGF-beta(1)), basic fibroblast growth factor (bFGF), Flt-1, and Flk-1 mRNA were analyzed from the left gastrocnemius by quantitative Northern blot. Ethanol increased VEGF, TGF-beta(1), bFGF, and Flt-1 mRNA at rest and after acute exercise. Ethanol increased resting Flk-1 mRNA. Ethanol increased bFGF mRNA independently of exercise. These findings suggest that 1) ethanol can increase skeletal muscle angiogenic growth factor gene expression and 2) the mechanisms responsible for the ethanol-induced increases in VEGF, TGF-beta(1), and Flt-1 mRNA appear to be different from those responsible for exercise-induced regulation.

Therefore, these results provide evidence in adult rat tissue that the protective cardiovascular effects of moderate ethanol consumption may result in part through the increase of angiogenic growth factors.

Med Hypotheses 2001 Sep;57(3):405-7
Does regular ethanol consumption promote insulin sensitivity and leanness by stimulating AMP-activated protein kinase?

McCarty MF.

Pantox Laboratories, San Diego, California 92109, USA.

There is good reason to believe that regular moderate alcohol consumption promotes insulin sensitivity of skeletal muscle; conceivably, this benefits the protective effects of moderate drinking on vascular health and risk for obesity and diabetes. The mechanism responsible for alcohol's insulin-sensitizing activity remains obscure. As a working hypothesis, it is proposed that metabolism of acetate in peripheral tissues generates sufficient levels of AMP to temporarily stimulate the AMP-activated protein kinase, which in turn induces the synthesis of certain long-lived proteins that act to boost insulin sensitivity and possibly aid the efficiency of fat oxidation as well.

Med Hypotheses 2000 May;54(5):794-7
The insulin-sensitizing activity of moderate alcohol consumption may promote leanness in women.

McCarty MF.

Pantox Laboratories, San Diego, USA.

Cross-sectional epidemiology reveals that women who drink alcohol regularly and moderately, on average, tend to have a decidedly lower body-mass index (BMI) than non-drinking women, despite slightly higher caloric intakes. In men, moderate drinkers are no heavier than non-drinkers, yet they consume considerably more calories. The thermogenic effect which this implies is not explained by the modest acute thermic effect of ethanol ingestion. However, there is indirect evidence that regular alcohol consumption has an insulin-sensitizing effect on skeletal muscle that down-regulates insulin secretion. Decreased insulin activity on adipocytes and the liver may discourage fat storage and promote hepatic mechanisms of ketogenesis, gluconeogenesis, and associated thermogenesis, thus possibly accounting for the relative leanness of female drinkers. The possibility that prescribing moderate alcohol intake could aid weight control in non-drinking overweight females should receive clinical evaluation.
The impact of moderate drinking on risk for diabetes in women appears to be quite dramatic.