It has been determined in the course of research that undergoing a long-term high energy diet is accompanied with progressive changes in the functional status of liver with the increase of transaminase amplifiers (AST, ALT) and increase in the content of total and conjugared bilirubin. The signs of hyperlipidemia and hypocholesteremia have been revealed during studies of the lipid metabolism in rats under conditions of long-term high energy diet. Such results testify to the fact that long-term consumption of high energy food is accompanied with the signs of dyslipoproteinemia and with increase in the level of atherogenic lipoproteins (low-density lipoproteins), which may be the initial substrate for atherosclerotic lesion of arteries when penetrating into the vessel walls.

Furthermore, the long-term consumption of high energy food is attended with distinct changes in oxidative homeostasis in liver of the experimental animals. It has been determined that on the 6th week of high energy food consumption from the beginning of the experiment the content of conjugated dienes in liver of the experimental rats has increased by 1.6 times compared to the initial examination and remained at this level on the 9th and 12th week of the experiment. Changes in the content of Schiff’s bases in liver in the experimental rats under conditions of the high energy diet are characterized by the increase on the 3rd week of the experiment by 3.3 times when compared to the exmination on the 12th week of the experiment. The obtained results indicate that the long-term high energy diet may lead to the initiation of lipid peroxidation processes that are accompanied with the increase of the toxic metabolites content. Continuous accumulation of such compounds causes disorientation of macromolecules in cells, destabilization of cell membranes and thereby stipulates structural and functional changes in cells and even their destruction. Increase in enzyme activity of superoxide dismutase (SOD) at the initial stages of the experiment may be conditioned rather by the increased enzyme synthesis in response to the state of oxidative stress and directed to maintain physiological homeostasis. Decrease in such indicator at the end of the experiment may be explained either by enzyme modification by the active form of oxygen or by depletion of superoxide dismutase reserves that are used for free radicals neutralization. Decrease of catalase activity in liver of the experimental rats is rather the result of negative impact of the free-radical substrates, excessive accumulation of which has been caused by the long-term consumption of high energy food.

Therefore, the obtained results indicate that the long-term high energy diet is accompanied with the increase of free-radical oxidation processes and exhaustion of the antioxidant system in the liver cells. We have evaluated the biochemical measurements that reflect functional condition of the mentioned organ (ALT, AST, total and conjugated bilirubin) and it proved the development and progressive changes in the liver functioning in rats under conditions of high energy diet, which may be stipulated by the great number of lipid peroxidation products and active forms of oxygen. Moreover, changes in lipid metabolism (development of hyperlipidemia, hypocholesteremia, and atherogenic dyslipoproteinemia) were revealed which also have close cause-effect relations with the liver dysfunction and inherently related to the changes of oxidative status of hepatocytes.

Keywords: High-Calorie Diet, liver, pre-diabetic state

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