scholarly journals A gender-related defect in lipid metabolism and glucose homeostasis in peroxisome proliferator- activated receptor alpha- deficient mice.

1998 ◽  
Vol 102 (6) ◽  
pp. 1083-1091 ◽  
Author(s):  
F Djouadi ◽  
C J Weinheimer ◽  
J E Saffitz ◽  
C Pitchford ◽  
J Bastin ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Glucose Homeostasis ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Receptor Alpha ◽  
Related Defect ◽  
Deficient Mice

scholarly journals Ablation of Selenbp1 Alters Lipid Metabolism via the Pparα Pathway in Mouse Kidney

2021 ◽  
Vol 22 (10) ◽  
pp. 5334
Author(s):  
Yingxia Song ◽  
Atsushi Kurose ◽  
Renshi Li ◽  
Tomoki Takeda ◽  
Yuko Onomura ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Peroxisome Proliferator ◽  
Related Factors ◽  
Sod Activity ◽  
Peroxisome Proliferator Activated Receptor ◽  
C57bl Mice ◽  
Low Levels ◽  
Inducible Protein ◽  
Cytochrome P450 4A ◽  
Deficient Mice

Selenium-binding protein 1 (Selenbp1) is a 2,3,7,8-tetrechlorodibenzo-p-dioxin inducible protein whose function is yet to be comprehensively elucidated. As the highly homologous isoform, Selenbp2, is expressed at low levels in the kidney, it is worthwhile comparing wild-type C57BL mice and Selenbp1-deficient mice under dioxin-free conditions. Accordingly, we conducted a mouse metabolomics analysis under non-dioxin-treated conditions. DNA microarray analysis was performed based on observed changes in lipid metabolism-related factors. The results showed fluctuations in the expression of numerous genes. Real-time RT-PCR confirmed the decreased expression levels of the cytochrome P450 4a (Cyp4a) subfamily, known to be involved in fatty acid ω- and ω-1 hydroxylation. Furthermore, peroxisome proliferator-activated receptor-α (Pparα) and retinoid-X-receptor-α (Rxrα), which form a heterodimer with Pparα to promote gene expression, were simultaneously reduced. This indicated that reduced Cyp4a expression was mediated via decreased Pparα and Rxrα. In line with this finding, increased levels of leukotrienes and prostaglandins were detected. Conversely, decreased hydrogen peroxide levels and reduced superoxide dismutase (SOD) activity supported the suppression of the renal expression of Sod1 and Sod2 in Selenbp1-deficient mice. Therefore, we infer that ablation of Selenbp1 elicits oxidative stress caused by increased levels of superoxide anions, which alters lipid metabolism via the Pparα pathway.

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