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PLTP activity inversely correlates with CAAD: effects of PON1 enzyme activity and genetic variants on PLTP activity.
Kim, Daniel Seung; Burt, Amber A; Ranchalis, Jane E; Vuletic, Simona; Vaisar, Tomas; Li, Wan-Fen; Rosenthal, Elisabeth A; Dong, Weijiang; Eintracht, Jason F; Motulsky, Arno G; Brunzell, John D; Albers, John J; Furlong, Clement E; Jarvik, Gail P.
Afiliación
  • Kim DS; Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA Department of Biostatistics, University of Washington School of Public Health, Seattle, WA.
  • Burt AA; Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
  • Ranchalis JE; Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
  • Vuletic S; Northwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
  • Vaisar T; Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
  • Li WF; Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
  • Rosenthal EA; Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
  • Dong W; Northwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA Department of Human Anatomy and Histology and Embryology, Xi'an Jiaotong University School
  • Eintracht JF; Department of General Medicine, Virginia Mason Medical Center, Seattle, WA.
  • Motulsky AG; Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA.
  • Brunzell JD; Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
  • Albers JJ; Northwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
  • Furlong CE; Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA.
  • Jarvik GP; Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA.
J Lipid Res ; 56(7): 1351-62, 2015 Jul.
Article en En | MEDLINE | ID: mdl-26009633
Recent studies have failed to demonstrate a causal cardioprotective effect of HDL cholesterol levels, shifting focus to the functional aspects of HDL. Phospholipid transfer protein (PLTP) is an HDL-associated protein involved in reverse cholesterol transport. This study sought to determine the genetic and nongenetic predictors of plasma PLTP activity (PLTPa), and separately, to determine whether PLTPa predicted carotid artery disease (CAAD). PLTPa was measured in 1,115 European ancestry participants from a case-control study of CAAD. A multivariate logistic regression model was used to elucidate the relationship between PLTPa and CAAD. Separately, a stepwise linear regression determined the nongenetic clinical and laboratory characteristics that best predicted PLTPa. A final stepwise regression considering both nongenetic and genetic variables identified the combination of covariates that explained maximal PLTPa variance. PLTPa was significantly associated with CAAD (7.90 × 10(-9)), with a 9% decrease in odds of CAAD per 1 unit increase in PLTPa (odds ratio = 0.91). Triglyceride levels (P = 0.0042), diabetes (P = 7.28 × 10(-5)), paraoxonase 1 (PON1) activity (P = 0.019), statin use (P = 0.026), PLTP SNP rs4810479 (P = 6.38 × 10(-7)), and PCIF1 SNP rs181914932 (P = 0.041) were all significantly associated with PLTPa. PLTPa is significantly inversely correlated with CAAD. Furthermore, we report a novel association between PLTPa and PON1 activity, a known predictor of CAAD.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedades de las Arterias Carótidas / Polimorfismo de Nucleótido Simple / Arildialquilfosfatasa / Proteínas de Transferencia de Fosfolípidos Tipo de estudio: Observational_studies / Prognostic_studies / Risk_factors_studies Límite: Aged / Female / Humans / Male Idioma: En Revista: J Lipid Res Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Enfermedades de las Arterias Carótidas / Polimorfismo de Nucleótido Simple / Arildialquilfosfatasa / Proteínas de Transferencia de Fosfolípidos Tipo de estudio: Observational_studies / Prognostic_studies / Risk_factors_studies Límite: Aged / Female / Humans / Male Idioma: En Revista: J Lipid Res Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos