Article

Dietary fatty acids modulate liver mitochondrial cardiolipin content and its fatty acid composition in rats with non alcoholic fatty liver disease

INRA UMR 866, Dynamique Musculaire et Métabolisme, 34060, Montpellier, France.
Journal of Bioenergetics (Impact Factor: 3.21). 06/2012; 44(4):439-52. DOI: 10.1007/s10863-012-9448-x
Source: PubMed

ABSTRACT

No data are reported on changes in mitochondrial membrane phospholipids in non-alcoholic fatty liver disease. We determined the content of mitochondrial membrane phospholipids from rats with non alcoholic liver steatosis, with a particular attention for cardiolipin (CL) content and its fatty acid composition, and their relation with the activity of the mitochondrial respiratory chain complexes. Different dietary fatty acid patterns leading to steatosis were explored. With high-fat diet, moderate macrosteatosis was observed and the liver mitochondrial phospholipid class distribution and CL fatty acids composition were modified. Indeed, both CL content and its C18:2n-6 content were increased with liver steatosis. Moreover, mitochondrial ATP synthase activity was positively correlated to the total CL content in liver phospholipid and to CL C18:2n-6 content while other complexes activity were negatively correlated to total CL content and/or CL C18:2n-6 content of liver mitochondria. The lard-rich diet increased liver CL synthase gene expression while the fish oil-rich diet increased the (n-3) polyunsaturated fatty acids content in CL. Thus, the diet may be a significant determinant of both the phospholipid class content and the fatty acid composition of liver mitochondrial membrane, and the activities of some of the respiratory chain complex enzymes may be influenced by dietary lipid amount in particular via modification of the CL content and fatty acid composition in phospholipid.

4 Followers
 · 
26 Reads
  • Source
    • "Lionetti et al.[47]compared mitochondrial function and dynamics in Wistar rats fed with a lard or fish-based diet (40% energy from fat, fish fat from cod liver) for six weeks. That evaluation was similar to the one published by Aoun et al.[4]using a different experimental design (12 weeks treatment, calculated 51.8% energy from fat; lard or fish fat from tuna and sardine oils). They observed that fat quantity, not quality, had a more prominent increased effect on mitochondrial membrane fluidity and membrane potentials , but not oxygen consumption. "

    Full-text · Dataset · Jan 2016
  • Source
    • "Lionetti et al.[47]compared mitochondrial function and dynamics in Wistar rats fed with a lard or fish-based diet (40% energy from fat, fish fat from cod liver) for six weeks. That evaluation was similar to the one published by Aoun et al.[4]using a different experimental design (12 weeks treatment, calculated 51.8% energy from fat; lard or fish fat from tuna and sardine oils). They observed that fat quantity, not quality, had a more prominent increased effect on mitochondrial membrane fluidity and membrane potentials , but not oxygen consumption. "
    Dataset: Full text

    Full-text · Dataset · Jan 2016
  • Source
    • "Lionetti et al.[47]compared mitochondrial function and dynamics in Wistar rats fed with a lard or fish-based diet (40% energy from fat, fish fat from cod liver) for six weeks. That evaluation was similar to the one published by Aoun et al.[4]using a different experimental design (12 weeks treatment, calculated 51.8% energy from fat; lard or fish fat from tuna and sardine oils). They observed that fat quantity, not quality, had a more prominent increased effect on mitochondrial membrane fluidity and membrane potentials , but not oxygen consumption. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Human metabolic diseases can be mimicked in rodents by using dietary interventions such as high fat diets (HFD). Nonalcoholic fatty liver disease (NAFLD) develops as a result of HFD and the disease may progress in a manner involving increased production of oxidants. The main intracellular source of these oxidants are mitochondria, which are also responsible for lipid metabolism and thus widely recognized as important players in the pathology and progression of steatosis. Here, we review publications that study redox and bioenergetic effects of HFD in the liver. We find that dietary composition and protocol implementations vary widely, as do the results of these dietary interventions. Overall, all HFD promote steatosis, changes in β-oxidation, generation and consequences of oxidants, while effects on body weight, insulin signaling and other bioenergetic parameters are more variable with the experimental models adopted. Our review provides a broad analysis of the bioenergetic and redox changes promoted by HFD as well as suggestions for changes and specifications in methodologies that may help explain apparent disparities in the current literature.
    Full-text · Article · Jan 2016
Show more