Atkins' diet results in steatosis (diet carbohydrates aorta cholesterol aldolase)
Metabolic and antioxidative changes in liver steatosis induced by
high-fat, low-carbohydrate diet in rabbits.
Birkner E, Kasperczyk S, Kasperczyk A, Zalejska-Fiolka J,
Zwirska-Korczala K, Stawiarska-Pieta B, Grucka-Mamczar E
J Physiol Pharmacol. 2005 Dec ; 56 Suppl 6: 45-58
Significantly decreased amounts of carbohydrates and increase of fat in
diet (Atkins' diet, Jan Kwasniewski'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.
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