The Effect of Moderate Alcohol Intake on Serum Apolipoproteins A-I and A-II: A Controlled Study

JAMA The Journal of the American Medical Association (Impact Factor: 35.29). 06/1985; 253(19):2854-7. DOI: 10.1001/jama.1985.03350430066027
Source: PubMed


High serum concentrations of apolipoprotein (apo) A-I are associated with a decreased risk of coronary heart disease. To study the effect of alcohol intake on serum apo A-I and A-II concentrations, 24 healthy male drinkers (37.8 +/- 13.9 mL [1.3 +/- 0.5 oz] of ethanol per day, mean +/- SD) were randomized into treatment and control groups after a three-week baseline period. The treatment group abstained from all intake of alcohol for the six weeks following randomization and then reverted to its usual level of intake for a five-week period. The control group continued its usual level of drinking throughout the trial. The concentrations of apo A-I and apo A-II of abstainers decreased significantly compared with the corresponding changes in controls. After drinking was resumed, apo A-I and apo A-II concentrations were significantly increased in the treatment group compared with the corresponding changes in the control group. These results suggest that the association between moderate alcohol intake and reduced risk of coronary heart disease may be mediated in part by increased levels of serum apo A-I or apo A-II, or both.

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    • "Furthermore, there has been disagreement as to whether changes in serum apolipoprotein levels are the result of ethanol itself of other substances found in alcoholic beverages. Human studies across a range of alcoholic beverages such as red wine, beer, and grain liquor (Camargo et al., 1985; Masarei et al., 1986; Gottrand et al., 1999; Senault et al., 2000) have all found increases in apolipoproteins. In this study, we have extended that finding to a non-human primate model with strict experimenter-controlled diet and consumption of pure ethanol diluted to 4%. "
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    ABSTRACT: Serum protein profiles were examined in naïve, ethanol self-administering and ethanol abstinent cynomolgus monkeys (Macaca fasicularis) to search for differences in protein expression which could possibly serve as biomarkers of heavy ethanol consumption. Surface-enhanced laser desorption ionization time-of-flight (SELDI-ToF) mass spectrometry was used for proteomic profiling of serum. Two proteins were identified by SELDI-ToF to be increased in ethanol self-administering compared with abstinent animals. These proteins were identified to be apolipoprotein AI (Apo-AI) and apolipoprotein AII (Apo-AII) by peptide mass fingerprinting and comparison with spectra of purified human Apo-AI and AII proteins. Immunoblot analysis of Apo-AI and Apo-AII was performed on a separate group of animals (within-animal ethanol-naïve and self-administering) and confirmed a statistically significant increase in Apo-AII, while Apo-AI was unchanged. An open proteomic screen of serum and confirmation in a separate set of animals found Apo-AII to be increased in the serum of ethanol self-administering monkeys. These results are consistent with previous clinical studies of human ethanol consumption and serum apolipoprotein expression. Moreover, these results validate the use of non-human primates as a model organism for proteomic analysis of ethanol self-administration biomarkers.
    Alcohol and Alcoholism 05/2006; 41(3):300-5. DOI:10.1093/alcalc/agl021 · 2.89 Impact Factor
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    • "The increase in HDL-C and APO A1 levels, associated with alcohol intake, appears to account for approximately half of the cardioprotective effect of alcohol (Rimm et al. 1999; Paunio et al. 1996; Parker et al. 1996). Other results also show that apolipoprotein A1 (APO A1) levels rise with alcohol consumption, and it may protect against atherosclerosis even better than HDL-C does (Camargo et al. 1985). Clinical and experimental studies suggest that other lipid measurements and apolipoprotein levels could be important for atherogenicity (Avogaro et al. 1979; Fager et al. 1980). "
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    ABSTRACT: This work studied the effects of ethanol in the absence and presence of haloperidol under two experimental conditions. In protocol 1, rats were treated daily with ethanol (4 g/kg, p.o.) for 7 days, and received only haloperidol (1 mg/kg, i.p.) from the 8th day to the 14th day. In protocol 2, animals received ethanol, and the treatment continued with ethanol and haloperidol from the 8th day to the 14th day. Results show increases in alanine transaminase (ALT; 48% and 55%) and aspartate transaminase (AST; 32% and 22%) levels after ethanol or haloperidol (14 days) treatments, as compared with controls. Apolipoprotein A-1 (APO A1) levels were increased by haloperidol, after 7- (148%) but not after 14-day treatments, as compared with controls. Levels of lipoprotein (high-density lipoprotein (HDL-C)) tended to be increased only by ethanol treatment for 14 days. ALT (80%) and AST (43%) levels were increased in the haloperidol plus ethanol group (protocol 2), as compared with controls. However, an increase in APO A1 levels was observed in the haloperidol group pretreated with ethanol (protocol 1), as compared with controls and ethanol 7-day treatments. Triglyceride (TG) levels were increased in the combination of ethanol and haloperidol in protocol 1 (234%) and 2 (106%), as compared with controls. Except for a small decrease in haloperidol groups, with or without ethanol, as related to ethanol alone, no other effect was observed in HDL-C levels. In conclusion, we showed that haloperidol might be effective in moderating lipid alterations caused by chronic alcohol intake.
    Biochemistry and Cell Biology 05/2004; 82(2):315-20. DOI:10.1139/o03-081 · 2.15 Impact Factor
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