title: Prediction of genetic risk for dyslipidemia.
abstract: The purpose of the present study was to identify genetic variants that confer susceptibility to dyslipidemia. A total of 5213 individuals from two independent populations were examined: Subject panel A comprised 3794 individuals who visited participating hospitals; subject panel B comprised 1419 community-dwelling elderly individuals. The genotypes for 100 polymorphisms of 65 candidate genes were determined. The chi(2) test and multivariable logistic regression analysis revealed that seven polymorphisms of APOA5, APOC3, APOA1, ACAT2, and LPL were significantly associated with hypertriglyceridemia, six polymorphisms of APOA5, LIPC, and CYP3A4 with low HDL-cholesterol, and three polymorphisms of APOE and CCR2 with high LDL-cholesterol in subject panel A. For validation of these associations, the same polymorphisms were examined in subject panel B. Six polymorphisms of APOA5, APOC3, APOA1, and LPL were again significantly associated with hypertriglyceridemia, three polymorphisms of APOA5 with low HDL-cholesterol, and two polymorphisms of APOE with high LDL-cholesterol. Serum triglyceride, HDL-cholesterol, and LDL-cholesterol concentrations differed significantly among genotypes of these corresponding polymorphisms in both subject panels. These results indicate that polymorphisms of APOA5, APOC3, APOA1, and LPL are determinants of hypertriglyceridemia and that those of APOA5 and APOE are determinants of low HDL-cholesterol and high LDL-cholesterol, respectively, in Japanese individuals.
authors.affiliation: Department of Human Functional Genomics, Life Science Research Center, Mie University, Tsu, Mie 514-8507, Japan. yamada@gene.mie-u.ac.jp
authors.forename: Yoshiji
authors.initials: Y
authors.lastname: Yamada
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Matsuo
authors.forename: Shunichiro
authors.initials: S
authors.lastname: Warita
authors.forename: Sachiro
authors.initials: S
authors.lastname: Watanabe
authors.forename: Kimihiko
authors.initials: K
authors.lastname: Kato
authors.forename: Mitsutoshi
authors.initials: M
authors.lastname: Oguri
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Yokoi
authors.forename: Norifumi
authors.initials: N
authors.lastname: Metoki
authors.forename: Hidemi
authors.initials: H
authors.lastname: Yoshida
authors.forename: Kei
authors.initials: K
authors.lastname: Satoh
authors.forename: Sahoko
authors.initials: S
authors.lastname: Ichihara
authors.forename: Yukitoshi
authors.initials: Y
authors.lastname: Aoyagi
authors.forename: Akitomo
authors.initials: A
authors.lastname: Yasunaga
authors.forename: Hyuntae
authors.initials: H
authors.lastname: Park
authors.forename: Masashi
authors.initials: M
authors.lastname: Tanaka
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Nozawa
mesh_terms: D000368:Aged; D001053:Apolipoproteins / Q000235:genetics*; D015415:Biomarkers; D008076:Cholesterol, HDL / Q000235:genetics*; D008078:Cholesterol, LDL / Q000235:genetics*; D015331:Cohort Studies; D050171:Dyslipidemias / Q000235:genetics*; D005260:Female; D005838:Genotype; D006801:Humans; D008055:Lipids / Q000097:blood; D008071:Lipoprotein Lipase / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D001053:Apolipoproteins; D015415:Biomarkers; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008055:Lipids; D008071:Lipoprotein Lipase