British Journal of Nutrition

Research Article

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

Marie-Soleil Gauthiera1, Roland Faviera2 and Jean-Marc Lavoiea1 c1

a1 Département de kinésiologie, Université de Montréal, C.P. 6128, Succ. centre-ville, Montréal, Québec, Canada H3C 3J7

a2 Équipe Mixte INSERM 221, Laboratoire de Bioénergétique Fondamentale et Appliquée, Université Joseph Fourier, Grenoble, France


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.

(Received June 02 2005)

(Revised August 31 2005)

(Accepted September 28 2005)


c1 *Corresponding author: Dr Jean-Marc Lavoie, fax +1 514 343 2181, email