Introduction: Studies have shown that an increase in carcinoembryonic antigen (CEA) is associated with the progression of colorectal cancer and is considered a sensitive diagnostic factor for CRC. Moreover, the role of peroxisome proliferators (PPARs) has recently been considered in colorectal cancer. This study aimed to investigate the relationship between the expression level of PPARs and CEA level in patients with colorectal cancer. Material & Methods: In this study, a total of 100 samples of primary tumor tissue along with adjacent healthy tissue samples and serum samples of patients with colorectal cancer who underwent surgery were prepared from the tumor bank of Tehran Cancer Institute in Thran, Iran. The expression level of peroxisome proliferator receptors (PRARs) in tissue samples and CEA level in serum samples were measured, and the relationship between these markers was evaluated as well. The financial support for the study was provided by the Islamic Azad University (grant number 132655). (Ethic code: 132655) Findings: The results of this study showed a significant increase in the expression level of PPARs and serum CEA levels in patients with colorectal cancer (P<0. 01). Although the level of these markers had a significant relationship with the progression and spread of disease in patients (P<0. 01), no significant relationship was observed between the expression of PPARs and serum CEA in these patients (P>0. 05). Discussion & Conclusion: Based on the obtained results, the expression level of PPARs and the serum CEA level are associated with the progression and spread of the disease,however, there is no significant relationship between the expression level of PPARs and the serum CEA level in patients with colorectal cancer.

Background: Peroxisome Proliferators- Activated Receptor-Gamma2 (PPAR-g2) is a nuclear receptor that regulates adipocyte differentiation, lipid metabolism and insulin sensitivity. The aim of this study was to evaluate the association of the Pro12Ala polymorphism at the PPAR-g2 gene in Iranian population with obesity.Methods: The genomic DNAs of the 156 subjects including obese and healthy isolated from EDTA whole blood. Pro12Ala polymorphism detected by Polymerase Chain Reaction – Restriction Fragment Length polymorphism (PCR-RFLP).Results: In the obese group, one sample (1.3%) was as homozygote Ala/Ala genotype, 24 samples (30.8%) were Pro/Ala heterozygote and 53 samples (67.9%) as Pro/Pro genotype were identified. in the control group, one sample (1.3%) was as Ala/Ala genotype, 12 samples (15.4%) were Pro/Ala genotype and 65 samples (83.3%) were Pro/Pro genotype. allele frequencies of  Ala in obese subjects (qAla=%16.7)were significantly different from those in control subjects (qAla=%8.9).Conclusion: Our results revealed that Pro12Ala polymorphism in PPAR-g2 gene associated with obesity in the Iranian population and presence Ala allele cause to significantly higher BMI and lower fasting blood sugar.

Background and purpose: Peroxisome proliferation-activated receptors (PPARg) are a class of ligand-dependent nuclear receptors, which act as transcription factors. In fact, the increased activity of PPARγ, can increase the expression and secretion of adiponectin but in patients with coronary artery disease these levels are reduced. This study was conducted to investigate the effect of omega-3 and vitamin E on the expression of this gene.Materials and methods: This double-blind, parallel clinical trial was conducted on 62 patients with coronary artery disease in Cardiovascular Research Center of Tehran in 2013. The patients were divided into three groups to receive n-3 fatty acids and n-3 and vitamin E combination therapy, and placebo (edible paraffin) for 8 weeks. The PPARg expression was investigated in peripheral blood mononuclear cell (PBMC) at first and after 8 weeks. As well as, Consumption data and statistical tests were analyzed using Nutritionist IV and SPSS V.18, respectively.Results: At the end of the study, the PPARg gene expression in PBMC significantly increased in the groups receiving n-3 fatty acids and n-3 and vitamin E combination therapy compared with baseline (P=0.029 and P=0.038, respectively). Also, significant differences were observed between the three groups (P=0.027) Conclusion: During eight weeks of treatment, the expression of PPARg in the groups receiving omega-3 fatty acids with or without vitamin E increased in patients with coronary artery disease.

Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors comprising three different isotypes termed b/d, a and g. They act at the transcriptional level. PPARg is expressed primarily in adipose tissue primarily in adipose tissue and is considered as an adipogenic factor which regulates the expression of genes associated with lipid metabolism. The ligand activated nuclear receptor peroxisome proliferator-activated receptor gamma (PPARg) has been shown to regulate cell activation, differentiation, proliferation, and/or apoptosis. Alternative promoter regions within the PPARg gene are responsible for the formation of three PPARg isoforms. Occurrence of (Pro12Ala) polymorphism was found to be significantly associated with a change in lipid profile in obese carrier individuals. PPARg is the target of the insulin sensitizing thiazplidinediones (TZDs), a class of currently used drugs in the treatment of type2 diabetes mellitus. PPARg plays a major role in tissue differentiation. The repressive effects of PPARg on tumor carcinoma cell lines have opened new hopes for therapeutic applications of this factor to inhibit the progress of cancer.

Background: Peroxisome Proliferator Activated Receptor gamma (PPARg), a member of nuclear receptor superfamily, comprises two isoforms in mouse.These two isoforms are encoded by different mRNAs, which are arisen by alternative promoter usage. There are two promoter regions upstream of PPARg gene. A 3 kb fragment, containing several transcription factor binding sites, acts as PPARg1 promoter region. Thus, expression pattern of PPARg1 isoform is due to the potential transcription factors that could influence its promoter activity. PPARg, Retinoid X Receptor (RXR) and Vitamin D Receptor (VDR), as nuclear receptors could influence PPARg gene expression pattern during several differentiation processes. During neural differentiation, PPARg1 isoform expression reaches to maximal level at neural precursor cell formation.Methods: A vast computational analysis was carried out to reveal the PPARg1 promoter region. The putative promoter region was then subcloned upstream of an EGFP reporter gene. Then the functionality of PPARg1 promoter was assessed in different cell lines.Results: Results indicated that Rosiglitazone increased PPARg1 promoter regulated EGFP expression of neural precursor cells during Embryoid Body (EB) formation. Furthermore vitamin D reduced PPARg1 promoter regulated EGFP expression of neural precursor cells during EB formation through binding to its receptor.Conclusion: This study suggests that there are potential response elements for PPAR/RXR and VDR/RXR heterodimers in PPARg1 isoform promoter. Also VDR/RXR heterodimers may decrease PPARg expression through binding to its promoter.

Melanoma is a challenging disease to treat. Punica granatum L. has a potential anticancer effect. This study determined the antiproliferative and antiangiogenic potential of the extract from pomegranate pericarp (PPE) in melanoma. Melanoma cells (1 × 106) were injected to C57BL6 mice subcutaneously. On 8th day, mice were randomly divided into 9 groups. Group 1 was considered as control and received distilled water. Groups 2 to 5 received 50, 100, 200 or 400 mg/kg of standardized PPE, orally. Group 6 received 400 mg/kg PPE and PPAR-γ antagonist (T0070907, 5 mg/kg/day). Group 7 received 400 mg/kg PPE and PPAR-α antagonist (GW6471, 10 mg/kg/day). Groups 8 and 9 received PPAR antagonists alone. On the 16th day, mice were euthanized and the tumor samples were analyzed by immunohistochemistry staining for Ki-67 and CD31. Vascular endothelial growth factor (VEGF) plasma level was determined by ELISA. PPE at the doses of 50, 100, 200, and 400 mg/kg decreased tumor weight to 1. 28, 1. 03, 0. 82, and 0. 58 g, respectively, in comparison with 1. 46 g in control group. Tumor volume reduced to 2. 1, 1. 7, 1. 35 and 0. 95 cm3 at the mentioned doses, in comparison with 2. 4 cm3 in control group (P < 0. 05 for all groups). VEGF, Ki-67 and CD31 were decreased dose dependently in the treatment groups (P < 0. 05). PPARα and PPARγ antagonists significantly reduced the extract effects (P < 0. 05). It was concluded that PPE may have a potential implication in melanoma treatment through activation of PPARα and PPARγ receptors.