Metabolic syndrome has a high prevalence (about 22.4% in adult individuals) in developed countries. Inflammation due to obesity and fat accumulation is the most important factor in the progression of metabolic syndrome. In cells which have a receptor for insulin hormone, inflammatory mediators target the insulin signaling pathway and cause insulin resistance. Peroxisome proliferator-activated receptors are a group of ligand inducible transcription factors, whose activation can improve insulin resistance and their agonists such as Genistein, which seems to be useful in prevention of insulin resistance development. Genistein is one of the soy derived isoflavonoids that affects carbohydrate and lipid metabolism resulting in prevention of insulin resistance. The current narrative review has concentrated mainly on highlighting the usefulness of Genistein in the improvement of insulin resistance and therapeutic potential of it in both in-vitro and in-vivo models. Genistein can increase fatty acid β-oxidation, decrease lipogenesis and improve insulin resistance in hepatocytes. In adipocytes, Genistein prevents downregulation of adiponectin expression and facilitates the upregulation of adiponectin expression. In β-islet cells, Genistein initiates the special cascade which leads to proliferation of β cells, resulting in increased secretion of insulin. Based on findings of the studies, it can be concluded that Genistein can be a useful agent in prevention of de novo lipid synthesis as well as proliferation of β cells. In this way the development of metabolic syndrome can be prevented.

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Background: Emerging evidence indicates that metformin has anti-inflammatory effect; however, the results differ concerning randomized controlled trails of the effect of metformin on inflammatory markers in type 2 diabetes (T2D) patients. Objective: This study reassessed the data on the effect of metformin treatment on inflammatory markers in T2D patients through a systematic review and meta-analysis. Methods: A systematic search was performed in the PubMed, ISI Web of Science, EMBASE, Cochrane Library and Scopus databases to collect relevant published data up to September 2020. Data of each study was combined using random-effects model. Subgroup analysis was performed based on subgroups of the treatment duration, dose and target population. Results: Thirteen RCTs including 1776 participants with T2D were analyzed. Although CRP levels significantly decreased [SMD: –0.76 mg/L; 95% CI (–1.48, –0.049); P = 0.036] in patients with T2D following metformin treatment, circulating levels of TNF-α [SMD: –0.17 pg/mL; 95% CI (–0.55, 0.20); P = 0.37] and IL-6 [SMD: –0.06 pg/mL; 95% CI (–0.38, 0.25); P = 0.69] were insignificant after metformin treatment. Compared to treatment duration of less than 24 weeks, longer treatment duration (more than 24 weeks) was associated with reduced level of CRP. Relevance to Patient Care and Clinical Practice: Based on available evidence from RCTs in this meta-analysis, metformin decreased CRP level. However, strategies for the treatment of inflammation should focus on metformin in patients with T2D. Conclusion: The present study evidences that therapy with metformin can reduces CRP level significantly in T2D patients compared to other inflammatory markers.

І. Background: Prolonged excessive salt intake is an important risk factor for development of renal fibrosis. In the onset of renal tubular destruction, KIM-1 appears in urine. CHOP is an important apoptosis stimulator protein. The aim of present study was to investigate the effect of high salt diet in development of renal fibrosis through apoptosis.ІІ. Methods and results: The 25 male Wistar rats were divided randomly into five groups and treated with 0%, 0.5%, 1%, 1.2%, 1.5% of NaCl dissolved in distilled water for 8 weeks. For confirmation of renal tubular destruction, the urinary KIM-1 was measured. The slides of renal tissue were prepared and stained with Hematoxylin and Eosin and Masson´s Trichrome for fibrosis detection. To investigate the role of CHOP protein in development of renal tubulointerstitial destruction, the relative gene expression of CHOP in renal tissue was analyzed using qRT-PCR method.There was no significant differences in urea, creatinine and total protein concentration of rats received different concentrations of NaCl compared to the control group. Urinary KIM-1 and mRNA level of CHOP was found to be increased significantly in rats treated with 1.5% NaCl compared to the control group. Mild renal fibrosis was observed in the same group too.III. Conclusion: Excessive salt intake can lead to fibrosis through increasing the expression of apoptotic CHOP gene in renal tissue. KIM-1 can be detectable in urine long before the development of renal fibrosis.