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Metabolic syndrome is known as a frequent precursor of type 2 diabetes mellitus (T2D). This disease could affect 8% of the people worldwide. Given that pancreatic β‐cell dysfunction and loss have central roles in the initiation and progression of the disease, the understanding of cellular and molecular pathways associated with pancreatic β‐cell dysfunction can provide more information about the underlying pathways involved in T2D. Multiple lines evidence indicated that oxidative stress, microRNA, and long noncoding RNA play significant roles in various steps of diseases. Oxidative stress is one of the important factors involved in T2D pathogenesis. This could affect the function and survival of the β cell via activation or inhibition of several processes and targets, such as receptor‐signal transduction, enzyme activity, gene expression, ion channel transport, and apoptosis. Besides oxidative stress, microRNAs and noncoding RNAs have emerged as epigenetic regulators that could affect pancreatic β‐cell dysfunction. These molecules exert their effects via targeting a variety of cellular and molecular pathways involved in T2D pathogenesis. Here, we summarized the molecular aspects of pancreatic β‐cell dysfunction. Moreover, we highlighted the roles of oxidative stress, microRNAs, and noncoding RNAs in pancreatic β‐cell dysfunction.

Background:Investigations have attempted to modify the outcome of tubular injury by either ameliorating renal tubular damage or promoting tubular regeneration in the case of acute tubular necrosis. Objectives: We investigated the protective effect of Eprex an erythropoietin analogue on tubular injury induced by gentamicin (GM). Materials and Methods: Forty male Wistar rats were randomly divided into four groups. In group 1,rats were served as a sham group. In group 2, rats were injected intraperitoneally with 100 mg/kg of GM for 10 consecutive days (positive control group) and then were sacrificed. In group 3, rats received GM for 10 days then Eprex 100U/kg was injected intraperitoneally for the next 10 days and then they were sacrificed at the day 20th. In group 4 rats were injected a combination of GM (80 mg/kg) and Eprex 100U/kg intraperitoneally for 10 days and then were sacrificed. Results: The results indicated that, Eprex prevented the increase in serum creatinine (Cr) and blood urea nitrogen (BUN). The effect of Eprex on damage score, showed that co-administration of GM and Eprex (group 3 and 4) reduced the kidney tissue damage compared to positive control group (P<0.05). This result indicat that Eprex potentially can reduce or prevent the kidney tissue damage. Conclusions: Ameliorative effect of Eprex when the drug was given in combination with GM and also when the drug was applied after GM-induced tubular damage, revealed the renoprotective potency of Eprex. Eprex is a promising drug to prevent or attenuate tubular damage induced by GM or other nephrotoxic agents which act through the same mechanisms as gentamicin.

One of the factors involved in accelerated atherosclerosis in hemodialysis patients is dyslipidemia. In this study we considered factors involved in intensification of dyslipidemia in hemodialysis patients.This study was done on 36 maintenance hemodialysis patients. Serum lipoprotein (a), Triglyceride, Cholesterol, HDL-C,LDL-C and also serum Intact parathormone( iPTH), Calcium, Phosphorus, Magnesium were measured. In statistical analysis there was not any correlation between serum lipids and iPTH. There was not correlation between serum calcium with serum lipids (p>0.05). There was not correlation between CaxP product with serum lipids (p>0.05). There was a positive correlation between serum Magnesium and Lipoprotein(a) (P<0.05) and also positive correlation between serum magnesium with triglyceride level (P<0.05) was seen too. Magnesium doesn’t increase the lipoprotein synthesis. It may involve in the regulation of some enzymes responsible for lipoprotein synthesis. Correlation of serum magnesium with serum triglycerides can be due to changes in hepatic triglyceride metabolism. Lipoprotein(a) is a non traditional factor of premature atherosclerosis, its association with serum magnesium needs more attention in hemodialysis patients.