Literature DB >> 19520316

Fructose-induced increase in ethanol metabolism and the risk of Syndrome X in man.

Ugochukwu E Uzuegbu1, Innocent Onyesom.   

Abstract

Syndrome X is biochemically characterized by impaired glucose tolerance, hypertriacylglycerolemia, altered HDL-cholesterol content and high blood pressure. In different isolated studies, alcohol and fructose have been observed to increase the risk of Syndrome X. However, several reports have recognized the potential of fructose in stimulating the elimination of alcohol from the bloodstream, but the effects of such an anti-intoxicating property of fructose on the biochemical features of Syndrome X have remained scarce. Thus, in this study, oral fructose was used to increase the metabolism of alcohol and the associated changes in blood glucose, triacylglycerol, lipoprotein cholesterol and blood pressure were measured and used to classify subjects into the Syndrome X risk category. One gram of fructose/kg body weight was used to 'treat' the intoxication caused by 1.0 g (20%) ethanol/kg body weight administered to forty-five consenting male subjects in apparently good health. The subjects were light alcohol drinkers (<20 g/day) between the ages of 25 and 35 years. Results show that the administered dose of fructose significantly (P<0.05) reduced the duration of alcohol intoxication by 30.7%, and accelerated the elimination (metabolism) of alcohol from bloodstream by 44.7% (P<0.05). However, ethanol+fructose, increased the number of subjects with impaired glucose and triacylglycerol (TAG) levels to 13 (29%) and 43 (96%) from 8 (18%) and 37 (82%) induced by the ethanol dose alone. The TAG number is the summation of those with borderline high and high concentrations. Oral fructose-induced stimulation of alcohol oxidation from bloodstream also has the potential of increasing the risk of Syndrome X. Ways of curbing the metabolic syndrome associated with oral fructose should be explored, if its anti-intoxicating property and use is to be recognized and promoted.

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Year:  2009        PMID: 19520316     DOI: 10.1016/j.crvi.2009.01.007

Source DB:  PubMed          Journal:  C R Biol        ISSN: 1631-0691            Impact factor:   1.583


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