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streptozotocin, fatty acids, high-fat diet, insulin resistance

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Natrus, L., Osadchuk, Y., Labudzinskyi, D., Chaikovsky, Y., & Smirnov, A. (2019). THE PATHOGENETIC RATIONALE THE WAYS OF EXPERIMENTAL TYPE 2 DIABETES MELLITUS MODELING. Medical Science of Ukraine (MSU), 15(3-4), 10-18.


Relevance. When modeling experimental type 2 diabetes mellitus (T2DM), various schools and research groups receive significant variability in tissue changes, which is difficult to compare and extrapolate as a specific pathogenic or pharmacological effect. The lack of standard operating procedures agreed upon in the scientific community greatly complicates the interpretation of the result. Therefore, the creation of a uniquely pathogenetic animal model of CD2 in animals is an urgent task.

Objective. Determination of the complex of exogenous effects for the most efficient reproduction of the experimental model of T2DM in rats and the pathogenetic justification of the changes in the body to study the central mechanisms of homeostasis regulation and their pharmacological correction.

Materials and methods. T2DM was model in rats by feeding a high-fat diet (HFD) with additional streptozotocin induction. The model was evaluated by anthropometric measurements, studies of biochemical parameters, an insulin tolerance test, analysis of the spectrum of fatty acids in the composition of tissues. Statistical data processing was performed with using the IBM SPSS Statistics 23.

Results. The obtained data were compared with our studies of the lipid metabolism of patients with varying degrees of diabetic retinopathy on the background of T2DM and analysis of the information content of biochemical markers to assess lipid metabolic disturbances on the background of hyperglycemia in patients. It was found that the simulation in rats of experimental T2DM by a food load of HFD (45%) + fructose 20% for 3 months followed by a single induction of streptozotocin (25 mg/kg) causes changes in lipid and carbohydrate metabolism in animals similar changes which are in the human with a diagnosed long-term diabetes and the development of microvascular complications.

Conclusion. We determined the optimal combination of effects and developed a consistent experimental load scheme that allows us to obtain a symptom model of type 2 diabetes in an animal experiment. Using the diagnostic algorithm, which includes physiological and laboratory methods, the degree of damage to organs and systems was determined, a comparison was made with the level of metabolic disorders in patients with T2DM and people without diabetes. The given model is a pathogenetically grounded approach for further study of the central mechanisms of homeostasis regulation and their pharmacological correction
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