Purpose of the study. To carry out a comparative analysis of the intake effect of mineral waters (MW) of various physicochemical compositions, including those ones enriched in selenium, on the pathogenesis of metabolic syndrome (MS) in the experiment.
MATERIALS AND METHODS
The experiment was carried out on 68 male white rats aged 3 months, which were divided into 5 groups. Control groups: CG1 — 10 animals without exposure; CG2 — 14 animals with MS, received only drinking water. Experimental groups: EG1 — 14 rats with MS, received MW1 of chloride-sulfate sodium composition (Ivanovo region); EG2 — 15 animals, received MW2 of chloride-hydrocarbonate-sodium composition (Essentuki No. 4); EG3 — 15 animals, received MW2 enriched with selenium. MS was modeled by double injection of streptozotocin, intraperitoneally, 30 μg/kg, after 60 days of finding the animals on a hypercaloric diet.
RESULTS
According to the oral glucose tolerance test (GTT) in animals with MS, two variants of the glycemic response were identified, according to which two subgroups (SG) were identified in each group. In the 1st SG CG2 and EG1-3, a moderate increase in glucose at the 60th minute of GTT was revealed, which was 1.2 times higher than the glucose level at the 60th minute in CG1. In SG 2, an increase in glucose was noted at the 60th minute by 2.5—5.0 times, by the 120th minute of GTG the glucose level was higher than in CG1. In animals CG2, there was no decrease in glucose by the 120th minute, in contrast to EG1-3. The activity of blood α-amylase increased by 2 times was determined in animals CG2 compared to CG1, and in groups EG1 and EG2 the level of its activity approached the level of CG1.
CONCLUSION
In animals with MS, a decrease in the sensitivity of β-cells to the stimulating effect of glucose and the involvement of the exocrine pancreas in the pathological process was determined. Under the influence of therapeutic course drinking MW of different physicochemical composition in animals with MS in the experiment, the sensitivity of tissues to the stimulating hyperglycemic signal was restored to varying degrees and the increased activity of blood α-amylase decreased.
