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 and Aims: Small dense  low-density lipoproteins (sd-LDL) particles are smaller and heavier than typical LDL ones. They can penetrate into the endothelium of coronary arteries more easily because of their small size. Diabetes mellitus is accompanied by dyslipidemia such as increasing concentration of plasma very low density lipoprotein and sd-LDL. Peroxisome proliferator activated receptor γ (PPARγ ) can decrease the level of sd-LDL in plasma. Biochanin A (BCA), a natural compound, is a PPARγ agonist. The present study was designed to investigate the effect of BCA on sd-LDL-Clolesterol level in diabetic animals. Materials and Methods: Adult male rats (Wistar strain) were used as the animal models in this study. Animals were made diabetic by single intraperitoneal injection of Streptozotocin- Nicotinamide and then treated by 1 and 5 mg/kg of BCA for 28 days. Body weight and fasting blood glucose were also tested before and at the end of treatment. Furthermore, the size of LDL particles were measured by nondenaturing polyacrylamide gradient gel electrophoresis assay. Results: Results of the present study indicated that BCA administration at dose of 5mg/kg decreased fasting blood glucose level and increased body weight and diameter of LDL particles in diabetic animals significantly. Conclusions: BCA seems to be an appropriate agent in diabetes mellitus, because it improves the diabetic dyslipidemia, which is the most important complication in diabetic patients.

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.