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Time course of the development of non-alcoholic hepatic steatosis in response to high-fat diet-induced obesity in rats

Published online by Cambridge University Press:  08 March 2007

Marie-Soleil Gauthier ,
Roland Favier  and
Jean-Marc Lavoie
Marie-Soleil Gauthier
Affiliation:
Département de kinésiologie, Université de Montréal, C.P. 6128, Succ. centre-ville, Montréal, Québec, Canada H3C 3J7
Roland Favier
Affiliation:
Équipe Mixte INSERM 221, Laboratoire de Bioénergétique Fondamentale et Appliquée, Université Joseph Fourier, Grenoble, France
Jean-Marc Lavoie*
Affiliation:
Département de kinésiologie, Université de Montréal, C.P. 6128, Succ. centre-ville, Montréal, Québec, Canada H3C 3J7
*
*Corresponding author: Dr Jean-Marc Lavoie, fax +1 514 343 2181, email [email protected]
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Abstract

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The aim of the study was to characterize the time course of the development of high-fat diet-induced hepatic steatosis and its relation to body fat accretion and changes in plasma lipid profile. Female Sprague–Dawley rats were high-fat fed (HF; 42%, kJ) for 1, 2, 4, 6, 12 and 16 weeks and compared to standard fed rats (SD). Data obtained from HF rats were further analysed by classifying the animals into obesity-prone and obesity-resistant. In HF rats, liver lipid content increased rapidly by approximately 200% during the first 2 weeks, decreased almost to baseline levels between weeks 2 and 6, and re-increased by 17% between weeks 6 and 16 (P<0·05). Body weight, body fat accretion, plasma leptin, NEFA and glycerol concentrations were higher in HF than in SD rats (P<0·05). These higher values were established in 2 weeks and the differences between the groups did not further enlarge from weeks 2 to 16. Obesity-prone rats depicted higher body weight and body fat accretion than obesity-resistant and SD rats. Surprisingly, however, liver lipid content was the same in obesity-prone as in obesity-resistant rats as they were both higher than in SD rats (weeks 2 and 16; P<0·05). Our data support the hypothesis that the liver acts as a systemic buffer, largely increasing its lipid content in the early stage of high-fat feeding. Our results also suggest that the development of non-alcoholic hepatic steatosis is more linked to dietary fat ingestion than to body weight gain.

Keywords

Fatty liverIntra-abdominal fatPlasma lipid profileNAFLDObesity resistant
Type
Research Article
Information
British Journal of Nutrition , Volume 95 , Issue 2 , February 2006 , pp. 273 - 281
Copyright
Copyright © The Nutrition Society 2006

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