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ArtikelVitamin E dietary supplementation significantly affects multiple risk factors for cardiovascular disease in baboons  
Oleh: Rainwater, David L. ; Mahaney, Michael C. ; VandeBerg, John L. ; Wang, Xing Li
Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The American Journal of Clinical Nutrition vol. 86 no. 03 (Sep. 2007), page 597.
Topik: Vitamin E; HDL; high-density lipoprotein; antioxidants; paraoxonase; apo A-I; apolipoprotein A-I; baboons
Ketersediaan
  • Perpustakaan FK
    • Nomor Panggil: A07.K.2007.03
    • Non-tandon: 1 (dapat dipinjam: 0)
    • Tandon: tidak ada
    Lihat Detail Induk
Isi artikelBackground: Oxidative stress is a widely accepted risk factor for cardiovascular disease (CVD), but the CVD benefit of dietary antioxidants, such as vitamin E, is controversial. Objective: Therefore, we have investigated, in the baboon model, the effects of dietary vitamin E supplementation on risk factors for CVD. Design: Pedigreed baboons (n = 251) were fed 2 atherogenic diets, high in fat and cholesterol, that differed in vitamin E concentrations. After 7 wk on each diet, blood samples were taken, and a panel of CVD risk factor traits (ie, indicators of lipoprotein metabolism and oxidative stress) were measured. Results: Vitamin E supplementation caused significantly higher total antioxidant status (TAS) and lower oxidized LDL as expected. In addition, vitamin E caused 2 paradoxical effects on HDL metabolism: higher apolipoprotein A-I (apo A-I) concentrations and lower HDL sizes. We calculated a difference () variable for each trait as the value on the high-vitamin E diet minus that on the low-vitamin E diet and determined that several HDL concentration variables were significantly correlated with TAS, but only one, apo A-I, was independently correlated. Genetic analyses showed that 2 variables, paraoxonase and HDL2, were significantly heritable, but that neither TAS nor apo A-I were heritable. Conclusions: Thus, our data show that dietary vitamin E improves TAS and LDL quality. They also show 2 apparently paradoxical effects on HDL metabolism: lower HDL2, which is mediated by genes, and higher apo A-I, which is not. These effects have contrasting associations with CVD risk and may help account for the mixed results from clinical trials of dietary vitamin E.
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