title: Association of the A/T54 polymorphism in the intestinal fatty acid binding protein with variations in plasma lipids in the Framingham Offspring Study.
abstract: We investigated the potential role of the genetic variation at the intestinal fatty acid binding protein gene (FABP2) in influencing lipid levels in a representative sample of the Framingham Offspring Study participants (n=1930). In men, the T54 allele was associated with significantly higher LDL-cholesterol (3.47+/-0.83 vs. 3.36+/-0.83 mmol/l; P<0.047), and ApoB (1.04+/-0.23 vs. 1.01+/-0.24 g/l; P<0.020) after adjustment for familial relationship, age, BMI, smoking, alcohol intake and the use of beta-blockers compared with the A54 allele. This relationship with ApoB continued to be significant after adjustment for APOE genotype (P<0.034). In women, the T54 allele was associated with significantly higher total-cholesterol (5.32+/-1.01 vs. 5.17+/-0.98 mmol/l; P<0.049) and LDL-cholesterol (3.31+/-0.93 vs. 3.18+/-0.85 mmol/l; P<0.023) after adjustment for covariates and menopausal status, estrogen therapy and APOE genotype. In men, the T54 allele was associated with significantly higher levels of small VLDL and lower levels of large HDL. Moreover, there was no significant relationship between FABP2 alleles and lipoprotein diameter or the prevalence of coronary heart disease in both genders. Our data are consistent with the T54 IFABP increasing the flux of lipids through the enterocyte leading to an increase in chylomicron secretion.
authors.affiliation: Lipid Metabolism Laboratory, Jean Mayer-USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111, USA. jgalluzzi@hnrc.tufts.edu
authors.forename: J R
authors.initials: JR
authors.lastname: Galluzzi
authors.forename: L A
authors.initials: LA
authors.lastname: Cupples
authors.forename: J D
authors.initials: JD
authors.lastname: Otvos
authors.forename: P W
authors.initials: PW
authors.lastname: Wilson
authors.forename: E J
authors.initials: EJ
authors.lastname: Schaefer
authors.forename: J M
authors.initials: JM
authors.lastname: Ordovas
mesh_terms: D017677:Age Distribution; D000368:Aged; D000483:Alleles; D001053:Apolipoproteins / Q000097:blood; D002352:Carrier Proteins / Q000235:genetics*; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000453:epidemiology / Q000235:genetics*; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D005227:Fatty Acids / Q000378:metabolism*; D005260:Female; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D014644:Genetic Variation; D006801:Humans; D015994:Incidence; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins; D011110:Polymorphism, Genetic; D011336:Probability; D011446:Prospective Studies; D012307:Risk Factors; D017678:Sex Distribution; D025521:Tumor Suppressor Proteins
chemical_list: D001053:Apolipoproteins; D002352:Carrier Proteins; C493404:FABP2 protein, human; C107608:FABP7 protein, human; C493405:Fabp2 protein, mouse; D000071438:Fatty Acid-Binding Protein 7; D050556:Fatty Acid-Binding Proteins; D005227:Fatty Acids; D008055:Lipids; D008074:Lipoproteins; D009363:Neoplasm Proteins; D025521:Tumor Suppressor Proteins