title: Effect of apoC-III gene polymorphisms on the lipoprotein-lipid profile of viscerally obese men.
abstract: Abdominal visceral adipose tissue (AT) accumulation is associated with an atherogenic metabolic profile that includes increased plasma triglyceride (TG), low HDL cholesterol levels, and an insulin-resistant hyperinsulinemic state. Whereas the apolipoprotein (apo) C-III C3238G gene variant, often referred to as the SstI polymorphism, has been related to variations in plasma TG concentrations, another variation within the insulin responsive element (C-482T) of the apoC-III gene has been associated with greater glucose and insulin responses to an oral glucose tolerance test (OGTT); however, these results were obtained in nonobese individuals. We therefore investigated the effects of three apoC-III gene polymorphisms, namely SstI, C-482T, and T-455C, on fasting plasma lipoprotein-lipid levels and response to a 75 g OGTT in a sample of 122 viscerally obese men (abdominal visceral AT area >or=130 cm(2)). Among the three gene variants that were examined, the SstI variation was the only one found to be associated with hypertriglyceridemia. Indeed, S1/S2 heterozygotes (n = 24) were characterized by increased fasting plasma TG concentrations compared with S1/S1 homozygotes (n = 98) (mean +/- SD: 3.03 +/- 1.58 vs. 2.34 +/- 0.95 mmol/l respectively, P < 0.05). The higher TG concentrations in S1/S2 were associated with the presence of smaller, denser LDL particles compared with S1/S1 subjects (LDL peak particle diameter: 24.8 +/- 0.5 nm vs. 25.1 +/- 0.5 nm respectively, P < 0.05). Furthermore, there was no association between the response to the OGTT and any of the apoC-III gene variants (SstI, T-455C, or C-482T) examined. Results of the present study support the notion of a hypertriglyceridemic effect associated with the apoC-III SstI polymorphism that could modulate the magnitude of the dyslipidemic state in abdominally obese patients.
authors.affiliation: Department of Food Sciences and Nutrition, Laval University, Sainte-Foy, Québec, Canada, G1K 7P4.
authors.forename: Charles
authors.initials: C
authors.lastname: Couillard
authors.forename: Marie-Claude
authors.initials: MC
authors.lastname: Vohl
authors.forename: James C
authors.initials: JC
authors.lastname: Engert
authors.forename: Isabelle
authors.initials: I
authors.lastname: Lemieux
authors.forename: Alain
authors.initials: A
authors.lastname: Houde
authors.forename: Natalie
authors.initials: N
authors.lastname: Almeras
authors.forename: Denis
authors.initials: D
authors.lastname: Prud'homme
authors.forename: Andre
authors.initials: A
authors.lastname: Nadeau
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Despres
authors.forename: Jean
authors.initials: J
authors.lastname: Bergeron
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D000483:Alleles; D053305:Apolipoprotein C-III; D001056:Apolipoproteins C / Q000235:genetics*; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D005215:Fasting / Q000097:blood; D005787:Gene Frequency; D014644:Genetic Variation; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood; D008055:Lipids / Q000097:blood*; D008074:Lipoproteins / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood / Q000378:metabolism; D008297:Male; D015999:Multivariate Analysis; D009765:Obesity / Q000097:blood / Q000235:genetics*; D011110:Polymorphism, Genetic; D012044:Regression Analysis; D013997:Time Factors; D014280:Triglycerides / Q000097:blood / Q000378:metabolism; D014781:Viscera
chemical_list: D053305:Apolipoprotein C-III; D001056:Apolipoproteins C; D001786:Blood Glucose; D007328:Insulin; D008055:Lipids; D008074:Lipoproteins; D008077:Lipoproteins, LDL; D014280:Triglycerides