Metabolomics of the interaction between PPAR‐α and age in the PPAR‐α‐null mouse
Abstract Regulation between the fed and fasted states in mammals is partially controlled by peroxisome proliferator‐activated receptor‐α (PPAR‐α). Expression of the receptor is high in the liver, heart and skeletal muscle, but decreases with age. A combined 1H nuclear magnetic resonance (NMR) spectr...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Springer Nature
2009-04-01
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| Series: | Molecular Systems Biology |
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| Online Access: | https://doi.org/10.1038/msb.2009.18 |
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| _version_ | 1849225774401323008 |
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| author | Helen J Atherton Melanie K Gulston Nigel J Bailey Kian‐Kai Cheng Wen Zhang Kieran Clarke Julian L Griffin |
| author_facet | Helen J Atherton Melanie K Gulston Nigel J Bailey Kian‐Kai Cheng Wen Zhang Kieran Clarke Julian L Griffin |
| author_sort | Helen J Atherton |
| collection | DOAJ |
| description | Abstract Regulation between the fed and fasted states in mammals is partially controlled by peroxisome proliferator‐activated receptor‐α (PPAR‐α). Expression of the receptor is high in the liver, heart and skeletal muscle, but decreases with age. A combined 1H nuclear magnetic resonance (NMR) spectroscopy and gas chromatography‐mass spectrometry metabolomic approach has been used to examine metabolism in the liver, heart, skeletal muscle and adipose tissue in PPAR‐α‐null mice and wild‐type controls during ageing between 3 and 13 months. For the PPAR‐α‐null mouse, multivariate statistics highlighted hepatic steatosis, reductions in the concentrations of glucose and glycogen in both the liver and muscle tissue, and profound changes in lipid metabolism in each tissue, reflecting known expression targets of the PPAR‐α receptor. Hepatic glycogen and glucose also decreased with age for both genotypes. These findings indicate the development of age‐related hepatic steatosis in the PPAR‐α‐null mouse, with the normal metabolic changes associated with ageing exacerbating changes associated with genotype. Furthermore, the combined metabolomic and multivariate statistics approach provides a robust method for examining the interaction between age and genotype. |
| format | Article |
| id | doaj-art-7fd1df8b9ef84f619f302a0d68387315 |
| institution | Kabale University |
| issn | 1744-4292 |
| language | English |
| publishDate | 2009-04-01 |
| publisher | Springer Nature |
| record_format | Article |
| series | Molecular Systems Biology |
| spelling | doaj-art-7fd1df8b9ef84f619f302a0d683873152025-08-24T11:59:37ZengSpringer NatureMolecular Systems Biology1744-42922009-04-015111010.1038/msb.2009.18Metabolomics of the interaction between PPAR‐α and age in the PPAR‐α‐null mouseHelen J Atherton0Melanie K Gulston1Nigel J Bailey2Kian‐Kai Cheng3Wen Zhang4Kieran Clarke5Julian L Griffin6Department of Biochemistry & Cambridge Systems Biology Centre, University of CambridgeDepartment of Biochemistry & Cambridge Systems Biology Centre, University of CambridgeSelcia Ltd, Fyfield Business and Research ParkDepartment of Biochemistry & Cambridge Systems Biology Centre, University of CambridgeUniversity Laboratory of Physiology, University of OxfordUniversity Laboratory of Physiology, University of OxfordDepartment of Biochemistry & Cambridge Systems Biology Centre, University of CambridgeAbstract Regulation between the fed and fasted states in mammals is partially controlled by peroxisome proliferator‐activated receptor‐α (PPAR‐α). Expression of the receptor is high in the liver, heart and skeletal muscle, but decreases with age. A combined 1H nuclear magnetic resonance (NMR) spectroscopy and gas chromatography‐mass spectrometry metabolomic approach has been used to examine metabolism in the liver, heart, skeletal muscle and adipose tissue in PPAR‐α‐null mice and wild‐type controls during ageing between 3 and 13 months. For the PPAR‐α‐null mouse, multivariate statistics highlighted hepatic steatosis, reductions in the concentrations of glucose and glycogen in both the liver and muscle tissue, and profound changes in lipid metabolism in each tissue, reflecting known expression targets of the PPAR‐α receptor. Hepatic glycogen and glucose also decreased with age for both genotypes. These findings indicate the development of age‐related hepatic steatosis in the PPAR‐α‐null mouse, with the normal metabolic changes associated with ageing exacerbating changes associated with genotype. Furthermore, the combined metabolomic and multivariate statistics approach provides a robust method for examining the interaction between age and genotype.https://doi.org/10.1038/msb.2009.18functional genomicshepatic steatosismetabonomicsobesity |
| spellingShingle | Helen J Atherton Melanie K Gulston Nigel J Bailey Kian‐Kai Cheng Wen Zhang Kieran Clarke Julian L Griffin Metabolomics of the interaction between PPAR‐α and age in the PPAR‐α‐null mouse Molecular Systems Biology functional genomics hepatic steatosis metabonomics obesity |
| title | Metabolomics of the interaction between PPAR‐α and age in the PPAR‐α‐null mouse |
| title_full | Metabolomics of the interaction between PPAR‐α and age in the PPAR‐α‐null mouse |
| title_fullStr | Metabolomics of the interaction between PPAR‐α and age in the PPAR‐α‐null mouse |
| title_full_unstemmed | Metabolomics of the interaction between PPAR‐α and age in the PPAR‐α‐null mouse |
| title_short | Metabolomics of the interaction between PPAR‐α and age in the PPAR‐α‐null mouse |
| title_sort | metabolomics of the interaction between ppar α and age in the ppar α null mouse |
| topic | functional genomics hepatic steatosis metabonomics obesity |
| url | https://doi.org/10.1038/msb.2009.18 |
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