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Diabetes mellitus is a chronic metabolic disease with life-threatening complications. The International Diabetes Federation estimates that 285 million people, 6.4% of the world population, suffered from diabetes in 2010 and this prevalence will increase to 439 million people, 7.7% of the world population by 2030. The prevalence of type 2 diabetes continues to increase at an alarming rate around the world, with even more people being affected by pre diabetes. While the pathogenesis and long-term complications of type 2 diabetes are fairly well known, its treatment has remained challenging, with only half of the patients achieving the recommended hemoglobin A1c target. For these reasons, the development of new drugs for the treatment of diabetes mellitus has been focused and still it remains, extremely desirable.
Studies of the effects of vanadium compounds on living systems have been abundant in the last years, reflecting the interest that vanadium compound might have for their environment impact and prospective applications in therapeutics In present study, for the first time in literature, we estimated the outcome of vanadyl sulfate on metabolic parameters and the genes expression in type 2 diabetic model, simultaneously. The first series of findings showed that compared to controls, in non-treated diabetic rats, weight, glucose, TG, TC, insulin and insulin resistance were increased significantly (p-value <0.05) that indicated induction of type 2 diabetes in rats.
Further, the results of vanadyl effect on metabolic profiles and gene expression showed that vanadyl sulfate significantly reduced weight, insulin secretion, TNF-a genes expression, lipid profiles except HDL that we couldn’t find any significant change, and increased PPAR-? gene expression in VS-treated diabetic rats compared to the non-treated diabetic group. Although the exact mechanism for reducing effects of VS on metabolic profiles stay ambiguous, but it may be proposed that the inhibitory power of this compound on metabolic Reponses may be owing to their useful effect on the gene expression.
Contrary to our findings, some studies demonstrated that vanadyl sulfate did not modify insulin sensitivity, but increased triglyceride concentrations and other lipid parameters or failed to improve dyslipidemia in diabetic rats. In consistent to our findings, there are a number of studies which supported benefit of vanadium supplementation for perfection of lipid complaints. Soveid, et al. showed that oral vanadium administration to diabetics had lowering effects on lipid parameters, but unlike us, they showed that HDL-c levels have been increased with unaltered TG levels.
Our results, demonstrated that vanadyl sulfate reduced fasting glucose, insulin secretion and HOMA-IR, but increased insulin sensitivity significantly in VS- treated groups compared to non-treated diabetic rats. These outcomes were similar to Missaoui and et.al that showed vanadyl sulfate normalized plasma glucose and improved insulin sensitivity in STZ-experimental diabetes and induced beta cells proliferation and/or regeneration. Further, the influence of vanadyl administration were evaluated on PPAR-? and TNF-a genes expression in this study. The results were in line with other studies indicating the positive effect of this metal on the genes.But the difference between our work and others was that this was done in the liver tissue, for the first time.
Our study had some limitations. The main restriction of our study was the absence of measurements of circulating levels of vanadyl sulfate in animals due to financial limits. Really, owing to limited financial resource for this projects, we did not assess some markers. Therefore, measurement of inflammatory cytokines and biomarkers of oxidative stress after intervention are reasonable in forthcoming studies. It may be concluded that vanadyl sulfate should be imperative and beneficial molecule for the expansion of the therapeutic materials for improvement of metabolic profiles and inflammatory markers in diabetic patients. Undoubtedly, further studies are needed to reveal the potential and/or possible toxicity of this compound in long-term use.
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