High Dietary Fat and Selenium Concentrations Exert Tissue- And Glutathione Peroxidase 1-Dependent Impacts on Lipid Metabolism of Young-Adult Mice

Abstract

Background: Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid metabolism. Objective: The objective was to reveal impacts and mechanisms of a moderately high Se and a high fat intake on lipid metabolism in Gpx1 knockout (KO) and wild-type (WT) mice. Methods: The KO and WT mice (males, 12-wk-old, body weight = 24.8 ± 0.703 g) were allotted to 4 groups each (n = 5) and fed a sucrose-torula yeast basal diet (5% corn oil) supplemented with 0.3 or 1.0 mg (+Se) Se/kg (as sodium selenite) and 0% or 25% [high-fat (HF)] lard for 6 wk. Multiple physiological and molecular biomarkers (68) related to lipid metabolism and selenogenome expression in plasma, liver, and/or adipose tissue were analyzed by 2-way (+Se by HF) ANOVA. Results: Compared with the control diet, the +Se diet decreased (P < 0.05) body-weight gain and plasma and liver concentrations of lipids (22-66%) but elevated (≤1.5-fold, P < 0.05) adipose tissue concentrations of lipids in the WT mice. The +Se diet up- and downregulated (P < 0.05) mRNA and/or protein concentrations of factors related to lipogenesis, selenogenome, and transcription, stress, and cell cycle in the liver (26% to 176-fold) and adipose tissues (14% to 1-fold), respectively, compared with the control diet in the WT mice. Many of these +Se diet effects were different (P < 0.05) from those of the HF diet and were eliminated or altered (P < 0.05) by the KO. Conclusions: The +Se and HF diets exerted tissue-specific and GPX1 expression-dependent impacts on lipid metabolism and related gene expression in the young-adult mice. Our findings will help reveal metabolic potential and underlying mechanisms of supplementing moderately high Se to subjects with HF intakes.