Abstract
Background. Excessive consumption of sucrose or protein deficiency in the diet can induce metabolic disorders in the kidney, whose functioning requires significant ATP energy expenditure. The study investigated the levels of the purine nucleotides ATP, ADP, AMP, and the activity of the enzymes FoF1-ATPase, 5′-nucleotidase, and AMP deaminase in the kidneys of rats exposed to different levels of protein and sucrose in their diet. Materials and Methods. The research was conducted on white non-linear rats, which were kept under different dietary regimens for a period of 4 weeks. Quantitative evaluation of the ATP, ADP, and AMP content was performed by thin-layer chromatography on Silufol sheets. FoF1-ATPase activity was determined by the accumulation of Pi. 5′-nucleotidase activity was measured based on the amount of inorganic phosphorus released in AMP hydrolysis. AMP deaminase activity was determined by the accumulation of ammonia. Results and Discussion. Research results revealed that in the mitochondria of the animals’ kidneys under conditions of low-protein diet, a significant reduction in AMP content was observed compared to the control, while ATP and ADP content remained unchanged. Simultaneously, the activities of 5′-nucleotidase, AMP deaminase, and FoF1-ATPase in the kidneys of animals on a low-protein diet were maintained at control levels. However, in rats maintained on a low-protein/high-sucrose diet, depletion of all adenine nucleotides is observed against an increase in the hydrolytic activity of FoF1-ATPase, AMP deaminase, and 5′-nucleotidase activities. The 5′-nucleotidase activity in animals of this group reaches maximum values in comparison with the control, indicating an enhanced AMP degradation mediated by 5′-nucleotidase in the conditions of low-protein/high-sucrose diet consumption. Conclusion. Excessive sucrose consumption in the context of dietary protein deficiency is accompanied by a depletion of the adenine nucleotides pool in the mitochondrial fraction and a significantly increased activity of purine catabolism enzymes in the cytosolic fraction of rat kidneys. This may result in an imbalance in the energy supply of renal cells. The obtained results open up prospects for developing a strategy for correcting energy metabolism disorders in the conditions of nutritional imbalance.
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