Diabetes mellitus (DM) is a central public health problem impacting more than 400 million humhttp://wsx5customurl.comans worldwide. This metabolic disorder progressively drives chronic microvascular, macrovascular and neuropathic life-threatening problems. DM is happened because of a decrease in insulin secretion, harm to pancreatic β cells or insulin resistance connected to the nonuse of insulin. Type – I DM The immune system, by mistake, will attack the β cells of the pancreas, where genes play a vital role. The work was designed to determine the levels of anthropometric variables (age and BMI), immunological parameters (IL-27, IL-27 gene SNP), CCKBR and other biochemical parameters (HbA1C, cholesterol, triglyceride, HDL, LDL, VLDL, urea and creatinine) in sera of T1DM patients. The study contains 180 subjects who are split into two groups; the two groups are the healthy control group and the T1DM patients' group. The result recorded in this research showed a non-significant (p>0.05) difference between the control and patients in age, BMI, CCKBR, TRI, HDL, LDL, and VLDL. A very high significant elevation (P<0.001) has been observed in the level of IL-27, HbA1C, urea and creatinine; there is a highly significant increase (p<0.05) in cholesterol, the gene SNP study shows a significant association of IL27 rs153109 with T1DM was observed under the allele model (OR=2.124, 95% CI (1.349–3.345), P=0.00105), and genotype model in the dominant model (OR=1.00, 95% CI, P=0.0016), recessive model (OR=0.35, 95% CI ( 0.12–1.02), P=0.043) and homozygous model (OR=1.00, 95%, P=0.0037). The study it is cleared that T1DM affects the SNP gene used as a promoter to the excretion of IL-27 and increases its excretion. Lipid profile shows an effect on the level of glucose in the blood, and a high level of cholesterol may cause a severe problem if it is combined with T1DM. The elevated glucose level happens because T1DM affects the renal and causes extreme conditions like renal failure and other renal dysfunction diseases. Keywords: T1DM, CCKBR, genetic disease, IL-27, IL-27.
Introduction. The work presents the results of studying the effects of three new azoloazine derivatives on oxidative glucose metabolism in order to select substances with the most acceptable characteristics for further preclinical study as potential antitumor agents, including for breast cancer chemotherapy.Aim. The aim of the work is to identify the metabolic properties of new azoloazine derivatives in terms of their effect on glucose metabolism using a culture of MCF-7 tumor cells and Vero non-tumor cells.Material and Methods. The testing on cell cultures was the main method used in the work, and all tested compounds were applied in final concentrations from 2.5 μmol/L. The comparison drug was epirubicin in the same concentration. The biochemical techniques included the determination of lactate production using commercial Olvex Diagnosticum kits and the determination of oxygen consumption by cells using the Seahorse XFe24 Analyzer for cellular metabolism. The results were processed statistically.Results. Lactate production in MCF-7 and Vero cell cultures decreased by more than half in the presence of 3-Cyclohexyl4-oxoimidazo[5,1-d]-[1,2,3,5]tetrazine-8-N-piperidinyl-carboxamide, and oxygen consumption decreased by 19-40%, which was the maximum effect among the studied azoloazine derivatives. Diethyl ether of 4-aminoimidazo[5,1-c][1,2,4]triazine-3,8dicarboxylic acid and 4-Amino-8-ethoxycarbonyl-imidazo[5,1-c][1,2,4]triazine-3-N-(p-toluyl)carboxamide were similar in their metabolic effects to the comparison drug epirubicin. They reduced lactate production in MCF-7 and Vero cell culture by a third and by 21–22%, respectively. Oxygen consumption in MCF-7 cell culture decreased by 14–17%, in Vero cell culture it decreased by 18–24%.Conclusion. The data obtained allow us to consider the (3-Cyclohexyl-4-oxoimidazo[5,1-d]-[1,2,3,5]tetrazine-8-N-piperidinylcarboxamide as the leader among new azoloazine derivatives and recommend it for further preclinical study as a potential antitumor agent.
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