Relevance. Alloxan and streptozotocin are used for experimental modeling of hyperglycemia. Damaged β-cells with these compounds lead to the reduction of synthesis and secretion of the level of insulin in the blood, as a result of which animals develop hyperglycemia and diabetic syndrome, similar to insulin-dependent type 1 diabetes. One of the methodological approaches for assessing the degree and development of tissue damage of vital organs, including diabetes, is the study of their fatty acid composition. But for the planning of an experiment with type 1 diabetes, it is necessary to take into account the discrepancy between the data obtained on different models.
Objective. The aim of the work is to study the changes in the fatty acid composition of cardiomyocyte and hepatocyte lipids in type 1 diabetes of the rats which are created on different models: alloxan (Allox) and streptozotocin (STZ).
Material and methods. In the experiment, the model of type 1 diabetes was developed by the single-dose administration of streptozotocin (50 mg/kg) and alloxane monohydrate in a dose of 130 mg/kg to white rats. Their administration caused a persistent hyperglycemia (20-34 mmol/L) to the majority of experimental animals. Research of the contents of 9 most informative fatty acids (FA) in the composition of the myocardium and liver homogenate was carried out by gas-vapor chromatography in the experimental laboratory of Scientific research institute. The statistical significance of differences in the meanings of the groups of comparisons was estimated by the Student's t-criterion.
Results. In the Allox model, we discovered a significant (p<0,05) 2-fold decrease in the proportion of palmitic FA to 9,5±0,5% relative to the control group 18,6±1,0% and stearic liquid crystal to 5,5±0,6% relative to the control 11,1±1,0% in the hepatocytes than in to STZ model. Additionally, we observed, a 12-fold increase in the content of meristic FA and pentadecane FA from 0,1±0,05% in the control to 1,2 ±0,1% in rats with the Allox model of diabetes. Among the unsaturated FA a significant increase (p <0,05) of 2,4 times the growth of oleinic FA from 14,8±1,5% to 34,2±1,6%, and a significant (p<0,05) in 1,5 times reduction of arachidone FA from 30,1±1,5% in control to 19,6±1,0% in rats with diabetes in the liver could be noted.
A significant increase (p<0,05) of oleinic FA from 15,1±0,7 in the control to 33,1±1,5% and a decrease of 1,3 times the linoleic FA from 28,8±1,0% in control to 21,8±2,0% in the Allox model of rats with 1 type diabetes was showed in the myocardium. On the other hand, the STZ model rats increased the content of linoleic acid to 34,9±1,0%, which was a significant (p<0,05) difference with the control and Allox model.
It is believed that the discrepancy in data is due to different pathogenetic mechanisms of action of drugs on tissues, which become targets of damage.
Conclusions. The Allox model of type 1 diabetes shows the aggressive effects of high-level radicals and can be successfully used to study the mechanisms of oxidative stress, which necessarily occurs in conditions of hyperglycemia. The development of the STZ model of diabetes reflects the less awful effects of cell's damage, and such simulations should be used in the study of tissue and organ disorders that occur with prolonged and persistent hyperglycemia.
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