High Dietary Fat and Selenium Concentrations Exert Tissue- and Glutathione Peroxidase 1–Dependent Impacts on Lipid Metabolism of Young-Adult Mice
Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid metabolism. 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) a...
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| Published in | The Journal of nutrition Vol. 150; no. 7; pp. 1738 - 1748 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.07.2020
Oxford University Press American Institute of Nutrition |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3166 1541-6100 1541-6100 |
| DOI | 10.1093/jn/nxaa130 |
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| Abstract | Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid metabolism.
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.
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.
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.
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. |
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| AbstractList | 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. Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid metabolism.BACKGROUNDExcessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid metabolism.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.OBJECTIVEThe 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.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.METHODSThe 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.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.RESULTSCompared 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.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.CONCLUSIONSThe +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. Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid metabolism. 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. 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. 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. 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. 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. Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid metabolism. 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. 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. 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. 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. |
| Author | Zhao, Zeping Kim, Jonggun Lei, Xin Gen |
| Author_xml | – sequence: 1 givenname: Zeping surname: Zhao fullname: Zhao, Zeping organization: Department of Animal Science, Cornell University, Ithaca, NY, USA – sequence: 2 givenname: Jonggun surname: Kim fullname: Kim, Jonggun organization: Department of Animal Science, Cornell University, Ithaca, NY, USA – sequence: 3 givenname: Xin Gen surname: Lei fullname: Lei, Xin Gen email: xl20@cornell.edu organization: Department of Animal Science, Cornell University, Ithaca, NY, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32386229$$D View this record in MEDLINE/PubMed |
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| Snippet | Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid metabolism.... ABSTRACT Background Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body... Background Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid... Excessive dietary selenium (Se; 3 mg/kg) or fat (>25%) intakes and overproduction of glutathione peroxidase 1 (GPX1) adversely affect body lipid... |
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| SubjectTerms | Adipose tissue Animal Feed - analysis Animals Biochemical, Molecular, and Genetic Mechanisms Biomarkers Body weight Cell cycle Corn oil Diet Diet - veterinary Diet, High-Fat Dietary Fats - administration & dosage Dietary minerals Fat metabolism Gene expression Gene Expression Regulation, Enzymologic - drug effects Glutathione Glutathione peroxidase Glutathione Peroxidase - genetics Glutathione Peroxidase - metabolism Glutathione Peroxidase GPX1 Hepatocytes Intakes Lipid metabolism Lipid Metabolism - drug effects Lipids Lipogenesis Liver Male Metabolism Mice Mice, Knockout Oils & fats Peroxidase Selenium Selenium - administration & dosage Selenium - pharmacology Sodium selenite Sucrose Sugar Transcription Variance analysis Yeast Young adults |
| Title | High Dietary Fat and Selenium Concentrations Exert Tissue- and Glutathione Peroxidase 1–Dependent Impacts on Lipid Metabolism of Young-Adult Mice |
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