NAFLD (non-alcoholic fatty liver disease) is a common cause of chronic liver disease associated with the metabolic syndrome. Effective techniques are needed to investigate the potential of animal models of NAFLD. The present study aimed to characterize murine models of NAFLD by metabolic profiling of intact liver tissue. Mice of three strains (BALB/c, C3H and the novel mutant, Gena/263) were fed a control or high-fat diet. Biometric, biochemical and histological analysis demonstrated a spectrum of NAFLD from normal liver to steatohepatitis. Metabolic profiling of intact liver tissue, using 1H MAS (proton magic angle spinning) MRS (magnetic resonance spectroscopy), showed an increase in the total lipid-to-water ratio, a decrease in polyunsaturation indices and a decrease in total choline with increasing disease severity. Principal components analysis and partial least-squares discriminant analysis showed separation of each model from its control and of each model from the total dataset. Class membership from the whole dataset was predicted with 100% accuracy in six out of eight models. Those models with steatosis discriminated from those with steatohepatitis with 100% accuracy. The separation of histologically defined steatohepatitis from simple steatosis is clinically important. Indices derived from 1H MAS MRS studies may inform subsequent in vivo MRS studies at lower field strengths.
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Research Article|
February 02 2009
Phenotyping murine models of non-alcoholic fatty liver disease through metabolic profiling of intact liver tissue
Jeremy F. L. Cobbold;
*Department of Hepatology and Gastroenterology, Imperial College London, St Mary's Hospital Campus, London W2 1NY, U.K.
†Imaging Sciences Department, Imperial College London, Hammersmith Hospital Campus, London W12 0HS, U.K.
Correspondence: Dr Jeremy F. L. Cobbold (email [email protected]).
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Quentin M. Anstee;
Quentin M. Anstee
*Department of Hepatology and Gastroenterology, Imperial College London, St Mary's Hospital Campus, London W2 1NY, U.K.
‡MRC Mammalian Genetics Unit, MRC Harwell, Oxfordshire OX11 0RD, U.K.
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Robert D. Goldin;
Robert D. Goldin
§Department of Histopathology, Imperial College London, St Mary's Hospital Campus, London W2 1NY, U.K.
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Horace R. T. Williams;
Horace R. T. Williams
*Department of Hepatology and Gastroenterology, Imperial College London, St Mary's Hospital Campus, London W2 1NY, U.K.
†Imaging Sciences Department, Imperial College London, Hammersmith Hospital Campus, London W12 0HS, U.K.
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Helen C. Matthews;
Helen C. Matthews
*Department of Hepatology and Gastroenterology, Imperial College London, St Mary's Hospital Campus, London W2 1NY, U.K.
‡MRC Mammalian Genetics Unit, MRC Harwell, Oxfordshire OX11 0RD, U.K.
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Bernard V. North;
Bernard V. North
∥Statistical Advisory Service, Imperial College London, South Kensington Campus, London SW7 2AZ, U.K.
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Nathan Absalom;
Nathan Absalom
‡MRC Mammalian Genetics Unit, MRC Harwell, Oxfordshire OX11 0RD, U.K.
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Howard C. Thomas;
Howard C. Thomas
*Department of Hepatology and Gastroenterology, Imperial College London, St Mary's Hospital Campus, London W2 1NY, U.K.
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Mark R. Thursz;
Mark R. Thursz
*Department of Hepatology and Gastroenterology, Imperial College London, St Mary's Hospital Campus, London W2 1NY, U.K.
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Roger D. Cox;
Roger D. Cox
‡MRC Mammalian Genetics Unit, MRC Harwell, Oxfordshire OX11 0RD, U.K.
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Simon D. Taylor-Robinson;
Simon D. Taylor-Robinson
*Department of Hepatology and Gastroenterology, Imperial College London, St Mary's Hospital Campus, London W2 1NY, U.K.
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I. Jane Cox
I. Jane Cox
†Imaging Sciences Department, Imperial College London, Hammersmith Hospital Campus, London W12 0HS, U.K.
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Publisher: Portland Press Ltd
Received:
May 16 2008
Revision Received:
July 08 2008
Accepted:
August 12 2008
Accepted Manuscript online:
August 12 2008
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© The Authors Journal compilation © 2009 Biochemical Society
2009
Clin Sci (Lond) (2009) 116 (5): 403–413.
Article history
Received:
May 16 2008
Revision Received:
July 08 2008
Accepted:
August 12 2008
Accepted Manuscript online:
August 12 2008
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Citation
Jeremy F. L. Cobbold, Quentin M. Anstee, Robert D. Goldin, Horace R. T. Williams, Helen C. Matthews, Bernard V. North, Nathan Absalom, Howard C. Thomas, Mark R. Thursz, Roger D. Cox, Simon D. Taylor-Robinson, I. Jane Cox; Phenotyping murine models of non-alcoholic fatty liver disease through metabolic profiling of intact liver tissue. Clin Sci (Lond) 1 March 2009; 116 (5): 403–413. doi: https://doi.org/10.1042/CS20080159
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