Hyperlipidemias: Lairon D

Lopez-Miranda J, Williams C, Lairon D. · Lipids and Atherosclerosis Research Unit, Department of Medicine, Hospital Universitario Reina Sofía, University of Cordoba, Córdoba, Spain. · Br J Nutr. · Pubmed #17705891 No free full text.

Abstract: Most of diurnal time is spent in a postprandial state due to successive meal intakes during the day. As long as the meals contain enough fat, a transient increase in triacylglycerolaemia and a change in lipoprotein pattern occurs. The extent and kinetics of such postprandial changes are highly variable and are modulated by numerous factors. This review focuses on factors affecting postprandial lipoprotein metabolism and genes, their variability and their relationship with intermediate phenotypes and risk of CHD. Postprandial lipoprotein metabolism is modulated by background dietary pattern as well as meal composition (fat amount and type, carbohydrate, protein, fibre, alcohol) and several lifestyle conditions (physical activity, tobacco use), physiological factors (age, gender, menopausal status) and pathological conditions (obesity, insulin resistance, diabetes mellitus). The roles of many genes have been explored in order to establish the possible implications of their variability in lipid metabolism and CHD risk. The postprandial lipid response has been shown to be modified by polymorphisms within the genes for apo A-I, A-IV, A-V, E, B, C-I and C-III, lipoprotein lipase, hepatic lipase, fatty acid binding and transport proteins, microsomal triglyceride transfer protein and scavenger receptor class B type I. Overall, the variability in postprandial response is important and complex, and the interactions between nutrients or dietary or meal compositions and gene variants need further investigation. The extent of present knowledge and needs for future studies are discussed in light of ongoing developments in nutrigenetics.

Vialettes B, Reynier P, Atlan-Gepner C, Mekki N, Lesluyes-Mazzochi L, Luc G, Lairon D, Malthiery Y. · Service de Nutrition, Maladies Métaboliques, Endocrinologie, Hôpital Sainte Marguerite, Université de la Méditerranée, Marseille, France. · Br J Nutr. · Pubmed #10911769 No free full text.

Abstract: This present case report describes two siblings with severe type V hyperlipoproteinaemia, diagnosed very early in life and due to the combination of the common apolipoprotein (Apo) E2 allele and rare mutant variant of ApoE, ApoE3 (Arg 136-->Ser). Phenotyping of ApoE falsely identified E2/E2 phenotype. The presence of mutated ApoE was suspected on an unusual restriction polymorphism of a Hha 1 restriction site and confirmed by sequence analysis of the cloned polymerase chain reaction fragment of exon 4 and familial segregation study. The severity of the hypertriacylglycerolaemia was modulated by the lipid content of the diet. A low-fat diet enriched in medium-chain triacylglycerol (TAG) decreased but did not normalize plasma TAG levels in both affected patients of the pedigree. A standardized lipid-enriched test meal showed a marked impairment of TAG-rich lipoprotein (TRL) clearance, especially the exogeneous TRL bearing ApoB-48 which still represented 79% of total TRL 7 h after the fat load. Finally, differences between the male and female siblings with the existence of a consanguine relationship in their parents suggested the involvement of other genetic factors in modulating the severity of phenotypic expression. This observation reinforces the usefulness of genotyping of ApoE for the characterization of genetic hypertriacylglycerolaemia and selection of the appropriate diet and treatment.

Valero R, Lorec AM, Paganelli F, Beliard S, Atlan C, Lairon D, Vialettes B, Portugal H. · Service de Nutrition-Maladies Métaboliques-Endocrinologie, AP-HM, Hôpital Ste Marguerite, Université de la Méditerranée, CHU Marseille, BP 29-13274 Marseille Cedex 09, France. · Metabolism. · Pubmed #16253631 No free full text.

Abstract: The aim of this study was to test the hypothesis that fasting apoprotein B-48 level might be a surrogate marker of postprandial lipemia in evaluating the risk of coronary artery disease (CAD) in a population without frank abnormality in fasting lipid profile. One hundred twenty-three patients tested by coronary angiography were selected on the criteria of absence of treatment with hypolipidemic drugs, obvious hypertriglyceridemia (>2.85 mmol/L), or other conditions that may interfere with lipoprotein metabolism except diabetes. CAD was defined by more than 50% narrowing of vessel lumen, and its severity is determined by the number of arteries involved. Fasting apoprotein B-48 was measured by a competitive enzyme-linked immunosorbent assay method. There was no difference in fasting apoprotein B-48 levels between the groups with and without CAD (0.123+/-0.096 vs 0.136+/-0.125 microg/mL, respectively), whatever the sex or whether with or without diabetes. The apoprotein B-48 level was not related to the presence or the severity of CAD. There was also no correlation between fasting apoprotein B-48 levels and age, sex, body mass index, and usual fasting lipid parameters in both patients with and without angiographically proven CAD. Finally, among the features of metabolic syndrome, apoprotein B-48 was correlated with fasting triglyceride levels (r=0.357, P<.01) only. In conclusion, the present study shows that in the absence of any major fasting abnormality in plasma lipid parameters, fasting apoprotein B-48 level, which has been associated with postprandial hyperlipidemia, does not predict the risk of CAD.

Harbis A, Juhel C, Senft M, Lairon D. · Unit 476-INSERM (National Institute of Health and Medical Research), Marseille, France. · Lipids. · Pubmed #10419118 No free full text.

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