Abstract
Background. Due to the fact that it is not always possible to reproduce all known manifestations of carbohydrate and lipid metabolism disorders, for example, in rodents, it is necessary to verify individual pathogenetic links in animals when modeling the metabolic syndrome in order to select the most optimal natural biotropic factors for studying the effect on them.
 Aims: To analyze metabolic disorders in the modeling of metabolic syndrome of alimentary genesis in comparison with the combined effect of alimentary factor and chemical agents to select the most appropriate model in the study of natural and weak preformed physical factors.
 Materials and methods. Metabolic syndrome was modeled in 47 sexually mature outbred white male rats using a hypercaloric diet (HD) of various duration and medications. The first series was the 1st control group (CG1) and the 1st experimental group (EG1). They received HD during 180 days, they were withdrawn from the experiment 30 days after the cancellation of HD. The second series was the 2nd control group (CG2) and three experimental groups. They received HD for 60 days, where the 2nd group (EG2) in association with HD received Mercazolil (10 mg/kg of animal weight) intragastrically for 14 days starting from the 21st day; the 3rd group (EG3) had the same scheme of treatment as in EG2, besides, after taking Mercazolil, they were intramuscularly injected with Nitox 200 at 25 mg/kg once per day during 5 days. Animals of EG2 and EG3 were withdrawn from the experiment 60 days after ending of HD. Animals of the 4th experimental group (EG4) got HD and the same medicine as in EG3. They left the experiment 30 days after ending HD. The content of hormones and biochemical parameters of protein, fat, and carbohydrate in peripheral blood was evaluated using multiple inter-group comparisons and intra-group relationships by Spearmans rank correlation method.
 Results. There have been detected a large number of biochemical signs of dependence of metabolism regulation on leptin level after long-term HD (180 days), while there were fewer biochemical signs of protein exchange disorder less than with the combined use of HD (60 days) and drugs.
 Conclusion. It is more appropriate and promising to use a long-term HD as a model of MS close to the natural conditions of its formation, to study the influence of natural and weak preformed physical factors.
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