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 and Aims: Health injustice is defined as "unnecessary, preventable, unjustified and unfair health differences." One of the most important scientific sources on the prevention and management of urolithiasis are Cochrane reviews in this field. Given that the first step in eliminating health injustice is to identify the causes, the aim of the present study was to evaluate equity considerations in Cochrane reviews and the included primary studies on urinary stones.Methods: Cochrane reviews on kidney stones and ureteral stones were searched through the Cochrane Library. The included clinical trials in each of the reviews published after 2000 were also collected. Two different researchers reviewed all the included Cochrane reviews and primary studies. The researchers reviewed each PROGRESS criteria independently

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Background: Metabolically healthy obese (MHO) individuals appear to be protected or more resistant to the progression of obesityrelated metabolic disorders. Hormonal regulation associated with adipose or muscular tissues such as irisin and leptin may facilitate the healthy metabolic profile of MHO cases. In this case-control study, the differences between serum level of irisin was investigated in metabolically unhealthy obese (MUO) and metabolically healthy obese (MHO) individuals.Methods: The study participants included obese individuals with metabolic syndrome (MetS) (n=51) and 2 control groups that included weight matched cases without MetS (n=51) and normal weight cases without MetS (n=51). Diagnosis of MetS was made based on the Adult Treatment Panel III (ATPIII) criteria. Serum levels of leptin and irisin were determined by enzyme-linked immune-sorbent assay (ELISA) kit. Receiver Operator Characteristic (ROC) curve, multiple linear regression, and one-way ANOVA analysis were used in SPSS 16 software. Significant level was set at 0.05.Results: Based on the statistical analysis, serum levels of irisin were 2.91±1.6, 3.14±1.4, and 4.47±3.23 (ng/mL) in MUO, MHO, and nonobese metabolically healthy participants, respectively (P = 0.001). Also, serum levels of leptin were 14.06±12.4, 11.2±9.3, and 7.09±7.1 (ng/mL) in MUO, MHO, and nonobese metabolically healthy cases, respectively (p=0.002). After adjusting for demographic variables, a significant association was found between irisin and study groups (β = 0.77, P = 0.001), weight (β=-0.03, p=0.014), BMI (β=-0.11, p=0.006), TG (β=-0.003, p=0.025), fat mass (β=-0.04, p=0.046), and fat free mass (β=0.08, p=0.014). Conclusion:Obese patients with/without MetS had lower level of irisin than normal weight participants.