4.1 Article

Lipid metabolism in ethanol-treated rat pups and adults: Effects of folic acid

Journal

ALCOHOL AND ALCOHOLISM
Volume 43, Issue 5, Pages 544-550

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/alcalc/agn044

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Funding

  1. Direccion General de Investigacion Cientifica y Tecnica (DGICYT) [PM98-0159]

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Aims: In this study we determined whether a folic acid-supplemented diet could change hyperlipaemia provoked by chronic ethanol intake in adult and pup rats. Methods: Animals were randomized into eight groups (four adults and four pups): control groups, water and basic diet; alcohol groups, 20% ethanol and basic diet; alcohol folic acid groups, 20% ethanol and diet supplemented with folic acid; control folic acid groups, water and folic acid-supplemented diet. We determined serum and liver total cholesterol (Chol), HDL, triglycerides (TG), phospholipids (PL) and bile acids (BA) levels in all of the groups. Hydroxymethylglutaryl-CoA (HMG-CoA) reductase activity was also measured in the livers. Results: Ethanol-fed rats have higher serum HDL and PL levels in pups and higher serum LDL, TG and PL levels in adults than controls and supplemented animals with or without alcohol ingestion. Ethanol provokes an increase in hepatic Chol and BA, and a decrease in hepatic TG and PL in pups; in adults it also provokes an increase in hepatic Chol and BA and a significant increase in HMG-CoA reductase activity. Alcohol intake plus folic acid supplementation has no effects on these values except BA levels that were significantly higher, in both pups and adult rats, than in the control group. Conclusion: Despite the fact that alcohol intake provokes different lipid alterations in adults and in pups whose mothers drank ethanol, folic acid contributes to the alleviation of these adverse effects reducing HMG-CoA reductase activity in adult rats and, except BA levels, to normalizing lipids values due to the fact that folic acid acts as a choleretic compound. We can therefore assume that folic acid supplementation reduces alcohol-induced hypercholesterolaemia by decreasing synthesis and increasing catabolism.

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