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Originally published In Press as doi:10.1194/jlr.M700285-JLR200 on August 10, 2007

Papers In Press, published online ahead of print November 1, 2007
J. Lipid Res., doi:10.1194/jlr.M700285-JLR200
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Journal of Lipid Research, Vol. 48, 2506-2513, November 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Patient-Oriented and Epidemiological Research

Increased concentrations of circulating vitamin E in carriers of the apolipoprotein A5 gene –1131T>C variant and associations with plasma lipids and lipid peroxidation

Isabella Sundl1,*, Montse Guardiola1,{dagger}, Gholamali Khoschsorur§, Rosa Solà{dagger}, Joan C. Vallvé{dagger}, Gemma Godàs{dagger}, Lluís Masana{dagger}, Michaela Maritschnegg*, Andreas Meinitzer§, Nicolas Cardinault**, Johannes M. Roob{dagger}{dagger}, Edmond Rock**, Brigitte M. Winklhofer-Roob* and Josep Ribalta2,{dagger}

* Human Nutrition and Metabolism Research and Training Center, Institute of Molecular Biosciences, Karl-Franzens University, Graz, Austria
{dagger} Unitat de Recerca en Lípids i Arteriosclerosi, Facultat de Medicina, Hospital Universitari de Sant Joan de Reus, Universitat Rovira i Virgili, Institut de Recerca en Ciències de la Salut, Reus, Spain
§ Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University, Graz, Austria
** Unité des Maladies Métaboliques et Micronutriments, Institut National de la Recherche Agronomique-Theix, St. Genes Champanelle, France
{dagger}{dagger} Division of Clinical Nephrology and Hemodialysis, Department of Internal Medicine, Medical University, Graz, Austria

Published, JLR Papers in Press, August 10, 2007.

1 I. Sundl and M. Guardiola contributed equally to this work.

2 To whom correspondence should be addressed. e-mail: josep.ribalta{at}urv.cat


ABSTRACT

The aim of this study was to investigate the effects of the apolipoprotein A5 (APOA5) 1131T>C gene variant on vitamin E status and lipid profile. The gene variant was determined in 297 healthy nonsmoking men aged 20–75 years and recruited in the VITAGE Project. Effects of the genotype on vitamin E in plasma, LDL, and buccal mucosa cells (BMC) as well as on cholesterol and triglyceride (TG) concentrations in plasma and apolipoprotein A-I (apoA-I), apoB, apoE, apoC-III, and plasma fatty acids were determined. Plasma malondialdehyde concentrations as a marker of in vivo lipid peroxidation were determined. C allele carriers showed significantly higher TG, VLDL, and LDL in plasma, higher cholesterol in VLDL and intermediate density lipoprotein, and higher plasma fatty acids. Plasma {alpha}-tocopherol (but not {gamma}-tocopherol, LDL {alpha}- and {gamma}-tocopherol, or BMC total vitamin E) was increased significantly in C allele carriers compared with homozygote T allele carriers (P = 0.02), but not after adjustment for cholesterol or TG. Plasma malondialdehyde concentrations did not differ between genotypes. In conclusion, higher plasma lipids in the TC+CC genotype are efficiently protected against lipid peroxidation by higher {alpha}-tocopherol concentrations. Lipid-standardized vitamin E should be used to reliably assess vitamin E status in genetic association studies.

Supplementary key words polymorphism • single nucleotide polymorphism • {alpha}-tocopherol • {gamma}-tocopherol • triglycerides • cholesterol • plasma fatty acids • lipoproteins

Abbreviations: apoA-V, apolipoprotein A-V; APOA5, apolipoprotein A5; BHT, butylated hydroxytoluene; BMC, buccal mucosa cell; BMI, body mass index; IDL, intermediate density lipoprotein; SFA, saturated fatty acid; TG, triglyceride


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