title: Metabolic and antioxidative changes in liver steatosis induced by high-fat, low-carbohydrate diet in rabbits.
abstract: Significantly decreased amounts of carbohydrates and increase of fat in diet (Atkins' diet, Jan Kwaśniewski's diet) may interfere with liver metabolism because main source of liver energy are carbohydrates. Large amount of fatty acid in diet may induce overproduction of reactive oxygen species in mitochondria because of increased oxidation and may cause steatosis. The influence of high-fat, low-carbohydrate diet (contained 14 g% protein, 25 g% fat, 8 g% carbohydrate) and compared to usual habitual diet (13 g% protein, 3 g% fat, 28 g% carbohydrate) as a control on liver function was examined in adult male rabbits. Fodder and water was ad libitum. The experiment lasted 24 weeks. At the beginning and every six weeks rabbits were weighed and blood was taken. Plasma glucose and cholesterol concentration, activity of glutamate dehydrogenase, alanine and aspartate in plasma and liver did not change. Concentrations of triacylglycerols (TG) in plasma were lower in the study group. Activity of aldolase increased in plasma and in liver in the study group while activity of sorbite dehydrogenase decreased in plasma at the end of the experiment. Malondialdehyde (MDA) concentration increased in aorta with no changes in liver and erythrocytes. Activity of glutathione peroxidase increased in erythrocytes and liver while total SOD increased only in the liver. High-fat, low-carbohydrate diet despite the lack of growth of the body mass, modifies significantly the homeostasis of carbohydrates and antioxidants in liver and enhanced production of TG in this organ, resulting in its steatosis.
authors.affiliation: Department of Biochemistry, Medical University of Silesia, Zabrze, Poland.
authors.forename: E
authors.initials: E
authors.lastname: Birkner
authors.forename: S
authors.initials: S
authors.lastname: Kasperczyk
authors.forename: A
authors.initials: A
authors.lastname: Kasperczyk
authors.forename: J
authors.initials: J
authors.lastname: Zalejska-Fiolka
authors.forename: K
authors.initials: K
authors.lastname: Zwirska-Korczala
authors.forename: B
authors.initials: B
authors.lastname: Stawiarska-Pieta
authors.forename: E
authors.initials: E
authors.lastname: Grucka-Mamczar
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D050197:Atherosclerosis / Q000209:etiology; D001786:Blood Glucose / Q000502:physiology; D050260:Carbohydrate Metabolism / Q000502:physiology*; D050528:Diet, Carbohydrate-Restricted / Q000009:adverse effects*; D004041:Dietary Fats / Q000009:adverse effects*; D004195:Disease Models, Animal; D004912:Erythrocytes / Q000201:enzymology / Q000473:pathology; D005234:Fatty Liver / Q000503:physiopathology*; D005634:Fructose-Bisphosphate Aldolase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D008099:Liver / Q000473:pathology; D008111:Liver Function Tests; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D010088:Oxidoreductases; D011817:Rabbits; D013482:Superoxide Dismutase / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D004041:Dietary Fats; D014280:Triglycerides; D008315:Malondialdehyde; D010088:Oxidoreductases; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005634:Fructose-Bisphosphate Aldolase