6533b82afe1ef96bd128ba72

RESEARCH PRODUCT

Moderate consumption of beer reduces liver triglycerides and aortic cholesterol deposit in LDLr-/- apoB100/100 mice.

Pierre ClouetJoseph GrestiBastien MoindrotIsmaël MohamedPascal Degrace

subject

medicine.medical_specialtyApolipoprotein BAlcohol DrinkingCholesterol VLDLAortic DiseasesPalmitatesDown-RegulationAorta ThoracicMitochondria LiverPolymerase Chain ReactionPhosphatidylcholine-Sterol O-Acyltransferasechemistry.chemical_compoundMiceInternal medicinemedicineAnimalsRNA MessengerScavenger receptorChromatography High Pressure LiquidTriglyceridesApolipoproteins BbiologyTriglycerideCholesterolReverse cholesterol transportCholesterol HDLfood and beveragesBeerLipoprotein(a)Cholesterol LDLScavenger Receptors Class BAtherosclerosisMice Inbred C57BLEndocrinologychemistryLiverReceptors LDLLDL receptorbehavior and behavior mechanismsbiology.proteinlipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineOxidation-ReductionLipoproteinSterol Regulatory Element Binding Protein 2

description

This study was designed to address the effects of a moderate consumption of beer on serum and liver lipid parameters and on the development of aortic lesions in a mouse model associated with a human atherogenic lipoprotein profile. LDLr(-/-) apoB(100/100) mice received each day during 12 weeks either water, mild beer (0.570g of ethanol/kg of body weight) or ethanol-free beer in a single pure dose. Serum and liver lipid parameters were analyzed and atherosclerotic lesions were estimated in heart and aorta through their total cholesterol content. mRNA levels of enzymes and receptors involved in lipoprotein uptake, in fatty acid esterification and oxidation, and in reverse cholesterol transport were also measured in the liver. Serum glucose, triglyceride (TG) and cholesterol levels were altered neither by ethanol-free beer nor by mild beer. Nevertheless, both beer treatments significantly increased HDL-cholesterol (HDL-C) and VLDL-C levels by reference to controls with no change in LDL-C levels. Liver TG contents were significantly decreased by either beer treatment. Cholesterol accumulation was attenuated in the whole aorta of mice treated with mild beer at p<0.05 and not significantly with ethanol-free beer. Heart cholesterol contents were comparable in the three series. Among the genes studied, only scavenger receptor-B1 was downregulated by both beer-based beverages. LDL receptor related protein, lecithin-cholesterol acyltransferase and sterol regulatory element-binding protein 2 were downregulated only by mild beer. The expression of other genes assayed was not altered. When administered in chronic and moderate dose, unidentified components of beer may exert beneficial effects towards atherosclerosis development through alteration of lipoprotein metabolism in LDLr(-/-) apoB(100/100) mice. This effect was slightly amplified by the presence of ethanol in beer.

10.1016/j.atherosclerosis.2006.01.012https://pubmed.ncbi.nlm.nih.gov/16487531