Akademik Veri Yönetim Sistemi
Annals of Hepatology, cilt.18, sa.5, ss.715-724, 2019 (SCI-Expanded)
Introduction and Objectives: The objectives of this study were to investigate the underlying mechanism of PPARα, LXRα, ChREBP, and SREBP-1c at the level of gene and protein expression with high-energy diets in liver and skeletal muscle. Materials and methods: Metabolic changes with consumption of high fat (Hfat), high sucrose (Hsuc) and high fructose (Hfru) diets were assessed. Levels of mRNA and protein of PPARα, LXRα, ChREBP, and SREBP-1c were investigated. Body weight changes, histological structure of liver and plasma levels of some parameters were also examined. Results: In Hfru group, body weights were higher than other groups (P < 0.05). In liver, LXRα levels of Hsuc and Hfru groups were upregulated as 1.87 ± 0.30 (P < 0.05) and 2.01 ± 0.29 (P < 0.01). SREBP-1c levels were upregulated as 4.52 ± 1.25 (P < 0.05); 4.05 ± 1.11 (P < 0.05) and 3.85 ± 1.04 (P < 0.05) in Hfat, Hsuc, and Hfru groups, respectively. In skeletal muscle, LXRα and SREBP-1c were upregulated as 1.77 ± 0.30 (P < 0.05) and 2.71 ± 0.56 (P < 0.05), in the Hfru group. Protein levels of ChREBP (33.92 ± 8.84 ng/mg protein (P < 0.05)) and SREBP-1c (135.16 ± 15.57 ng/mg protein (P < 0.001)) in liver were higher in Hfru group. In skeletal muscle, LXRα, ChREBP and SREBP-1c in Hfru group were 6.67 ± 0.60, 7.11 ± 1.29 and 43.17 ± 6.37 ng/mg, respectively (P < 0.05; P < 0.01; P < 0.05). The rats in Hfru group had the most damaged livers. Conclusion: Besides liver, fructose consumption significantly effects skeletal muscle and leads to weight gain, triggers lipogenesis and metabolic disorders.