Endocrine Abstracts

The work was initiated to study some biochemical parameters in peripheral blood of animals upon diet-induced obesity and insulin resistance modeling. Obesity was induced in BALB/c mice by keeping them on the high- carbon diet for 13 weeks. The commercially available kits were used to assay glucose, alkaline phosphatase, creatine kinase and cholesterol; concentrations of testosterone were measured by the enzyme immunoassay. The high carbon diet in BALB/c mice served as a basis for the animal model with experimental obesity and insulin resistance. In the animals the diet-induced obesity was accompanied with body mass gain (by 48%), increase in the levels of glucose (6.68±0.94 versus 2.43±0.52 mmol/l in the control animals) and total cholesterol (2.02±0.52 versus 0.54±0.20 mmol/l in the control animals), and reduction in their insulin sensitivity. The high carbon diet used in the study was established to cause changes in blood serum biochemical parameters. The activities of alkaline phosphatase and creatine kinase were found to decline to be 64.9±7.88 IU versus 347.6±13.8 IU and 56.6±2.11 U/l versus 364.0±10.37 U/l in the controls, respectively. The changes could associate with injuries of hepatocytes due to type 2 diabetes mellitus onset. Concentrations of testosterone in the animals under study were found increased (66.05 nmol/l versus 34.33±3.38 nmol/l in the controls), and obesity, lipid metabolism disorders and insulin resistance are thought to induce the increase of the hormone in the experimental animals’ blood serum. All the changes above could be attributed to the compensatory mechanisms triggering restoration of functional and proliferative activity of hepatocytes. The 13-week high-carbon diet in BALB/c mice was shown to cause diet-induced obesity with insulin resistance accompanied by changes in some biochemical parameters of experimental animals’ blood.