Liver mitochondrial function and redox status in an experimental model of non-alcoholic fatty liver disease induced by monosodium l-glutamate in rats

The purpose of this work was to determine if mitochondrial dysfunction is involved in the development of non-alcoholic fatty liver disease (NAFLD). Using a model of obesity induced by the neonatal treatment of rats with monosodium l-glutamate (MSG), several parameters of liver mitochondrial function...

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Bibliographic Details
Published in:Experimental and molecular pathology 2011-12, Vol.91 (3), p.687-694
Main Authors: Lazarin, Murilo de Oliveira, Ishii-Iwamoto, Emy Luiza, Yamamoto, Nair Seiko, Constantin, Rodrigo Polimeni, Garcia, Rosângela Fernandes, da Costa, Cecília E. Mareze, Vitoriano, Adriana de Souza, de Oliveira, Monique Cristine, Salgueiro-Pagadigorria, Clairce L.
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Biological and medical sciences
Fatty Liver - chemically induced
Fatty Liver - complications
Fatty Liver - metabolism
Gastroenterology. Liver. Pancreas. Abdomen
Glucosephosphate Dehydrogenase - metabolism
Glutathione - metabolism
Glutathione Peroxidase - metabolism
Glutathione Reductase - metabolism
Investigative techniques, diagnostic techniques (general aspects)
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Male
Medical sciences
Metabolic diseases
Mitochondria
Mitochondria, Liver - metabolism
MSG
NAFLD
Non-alcoholic Fatty Liver Disease
Obesity
Obesity - chemically induced
Obesity - complications
Obesity - metabolism
Other diseases. Semiology
Oxidation-Reduction
Oxidative Phosphorylation
Oxidative stress
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
Rats
Rats, Wistar
ROS
Sodium Glutamate - toxicity
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Summary:The purpose of this work was to determine if mitochondrial dysfunction is involved in the development of non-alcoholic fatty liver disease (NAFLD). Using a model of obesity induced by the neonatal treatment of rats with monosodium l-glutamate (MSG), several parameters of liver mitochondrial function and their impact on liver redox status were evaluated. Specifically, fatty acid β-oxidation, oxidative phosphorylation and Ca 2+-induced mitochondrial permeability transition were assessed in isolated liver mitochondria, and reduced glutathione (GSH), linked thiol contents and the activities of several enzymes involved in the control of redox status were measured in the liver homogenate. Our results demonstrate that liver mitochondria from MSG-obese rats exhibit a higher β-oxidation capacity and an increased capacity for oxidising succinate, without loss in the efficiency of oxidative phosphorylation. Also, liver mitochondria from obese rats were less susceptible to the permeability transition pore (PTP) opening induced by 1.0 μM CaCl 2. Cellular levels of GSH were unaffected in the livers from the MSG-obese rats, whereas reduced linked thiol contents were increased. The activities of glucose-6-phosphate dehydrogenase, glutathione reductase and glutathione peroxidase were increased, while catalase activity was unaffected and superoxide dismutase activity was reduced in the livers from the MSG-obese rats. In this model of obesity, liver fat accumulation is not a consequence of mitochondrial dysfunction. The enhanced glucose-6-phosphate dehydrogenase activity observed in the livers of MSG-obese rats could be associated with liver fat accumulation and likely plays a central role in the mitochondrial defence against oxidative stress. ► Mitochondria. ► Liver. ► Redox status. ► MSG-obese rats.
ISSN:0014-4800
1096-0945
DOI:10.1016/j.yexmp.2011.07.003