Elsevier

Metabolism

Volume 38, Issue 2, February 1989, Pages 166-171
Metabolism

Short-term effects of moderate alcohol consumption on lipid metabolism and energy balance in normal men

https://doi.org/10.1016/0026-0495(89)90257-6Get rights and content

Abstract

The short-term effects of moderate alcohol consumption on energy balance, serum lipids, and lipoproteins were studied in eight healthy middle-aged men (age 30 to 47 years and body mass index 23.1 to 27.7 w/h2). A crossover dietary trial included two isocaloric periods without (20% protein, 50% carbohydrate, 30% fat) or with alcohol (12% protein, 29% carbohydrate, 25% fat, 75 g of alcohol as red wine). Each period lasted 2 weeks. The body weight of the subjects remained stable over the study. Fasting blood glucose, serum insulin, total cholesterol, and LDL cholesterol were similar at the end of both dietary periods. Mean values of serum total triglyceride (108 ± 18 v 85 ± 24 mg/dL, P < 0.05), VLDL-Tg (88 ± 24 v 73 ± 16 mg/dL, NS), and total HDL cholesterol (49.4 ± 6.0 v 43.4 ± 5.5 mg/dL, P < 0.05) were higher after the diet with alcohol than without alcohol. The increase of HDL cholesterol was primarily due to that of HDL2 cholesterol (10.4 ± 5.1 v 5.7 ± 3.9 mg/dL, P < 0.05). The concentration of apoprotein A-I, A-II, and B averaged 104 ± 17 v 89 ± 16 mg/dL, 33 ± 4 v 28 ± 8 mg/dL, P < 0.02, and 111 ± 24 v 105 ± 33 mg/dL after the diets with and without alcohol, respectively. Adipose tissue LPL activity increased in six of the eight volunteers during the diet with alcohol. Resting metabolic rate, postprandial energy expenditure, and postprandial responses of blood glucose, serum insulin, triglyceride, and plasma FFA were similar after the both diets. Moderate daily intake of alcohol (up to 75 g/d) as a part of an isocaloric diet has no major effect on energy balance or postprandial glucose response, but it induces changes in serum lipids and lipoproteins, particularly in HDL lipids and proteins.

References (54)

  • JRL Masarei et al.

    Effects of alcohol consumption on serum lipoprotein-lipid and apolipoprotein concentrations. Results from an intervention study in healthy subjects

    Atherosclerosis

    (1986)
  • NA Pikaar et al.

    Effect of moderate alcohol consumption on platelet aggregation, fibrinolysis, and blood lipids

    Metabolism

    (1987)
  • MR Taskinen et al.

    A micromethod for assay of lipoprotein lipase activity in needle biopsy samples of human adipose tissue and skeletal muscle

    Clin Chim Acta

    (1980)
  • AW Wahlefeld

    Triglyceride determination after enzymatic hydrolysis

  • LI Gidez et al.

    Separation and quantitation of subclasses of human plasma high density lipoproteins by a simple precipitation procedure

    J Lipid Res

    (1982)
  • GE Fraser et al.

    The effect of alcohol on serum high density lipoprotein (HDL). A controlled experiment

    Atherosclerosis

    (1983)
  • P Puchois et al.

    Serum apolipoprotein A-II, a biochemical indicator of alcohol abuse

    Clin Chim Acta

    (1984)
  • MC Cheung et al.

    Characterization of lipoprotein particles isolated by immunoaffinity chromatography

    J Biol Chem

    (1984)
  • MR Taskinen et al.

    Sequence of alcohol-induced initial changes in plasma lipoproteins (VLDL and HDL) and lipolytic enzymes in humans

    Metabolism

    (1985)
  • P Devenyi et al.

    High-density lipoprotein cholesterol in male alcoholics with and without severe liver disease

    Am J Med

    (1981)
  • T Sane et al.

    Accelerated turnover of very low density lipoprotein triglycerides in chronic alcohol users. A possible mechanism for the up-regulation of high density lipoprotein by ethanol

    Atherosclerosis

    (1984)
  • J Schneider et al.

    Lipoprotein fractions, lipoprotein lipase and hepatic triglyceride lipase during short-term and long-term uptake of ethanol in healthy subjects

    Atherosclerosis

    (1985)
  • MC Mitchell et al.

    Alcohol and nutrition: Caloric value, bioenergetics, and relationship to liver damage

    Annu Rev Nutr

    (1986)
  • N Melchionda et al.

    L'obesita nei soggetti anziani

  • M Välimäki et al.

    Comparison of the effects of two difference doses of alcohol on serum lipoproteins, HDL-subfractions and apolipoproteins A-I and A-II: a controlled study

    Eur J Clin Invest

    (1988)
  • WD Atwater et al.

    An experimental inquiry regarding the nutritive value of alcohol

    Mem Natl Acad Sci

    (1902)
  • EW Barnes et al.

    Observations on the metabolism of alcohol in man

    Br J Nutr

    (1965)
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    Supported by grants from the University of Helsinki and the Sigrid Juselius Foundation (M.R.T.), Helsinki, Finland.

    Deceased September 1986.

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