Lack of association between endothelial nitric oxide synthase glu298Asp variation, visceral obesity and insulin related phenotypes in Turkish type 2 diabetic patients

Nitric oxide (NO) is an endothelium derived relaxing factor (EDRF) important in regulating heart-vessel physiology. The objective of this study was to investigate whether the eNOS gene Glu298Asp variation influenced the lipid parameters, visceral obesity, insulin related phenotypes and type 2 diabetes mellitus (T2DM) development, for the first time in a Turkish study group. We analyzed the the eNOS gene Glu298Asp genotype frequencies in 115 type 2 diabetic and 68 healthy control subjects. Serum lipids and insulin-related phenotypes were also analyzed. No significant difference for genotypic frequencies was observed for the Ban II (Eco241) restriction site in T2DM patients as compared to controls. eNOS Glu298Asp polymorphism was not found to affect visceral obesity and insulin related phenotypes. However, T2DM patients with Asp/Asp genotype were found to have lower hepatic insulin sensitivity (HIS) in comparison to Glu/Glu. In healthy controls, the insulin and HOMA levels were found to be lower in Glu/Asp genotype with respect to Glu/Glu genotype carriers (p>0.05). In T2DM patients, visceral obesity was observed in higher frequencies with Asp/Asp genotype, in comparison to Glu/Glu genotype. eNOS Glu298Asp polymorphism was not found to affect serum lipid levels in the T2DM group. However in the control group, lower serum apoB levels were observed in Asp/Asp genotype carriers in comparison to Glu/Glu genotype (p ≤ 0.05). The eNOS gene Glu298Asp polymorphism was not found to be associated with T2DM in the present study group. Although not significant, since the eNOS Glu298Asp genotypes were found to be related to HIS, insulin, HOMA and visceral obesity in the present study, further studies on larger samples are needed to explore the exact role of eNOS Glu298Asp polymorphism in insulin related phenotypes and visceral obesit

Investigation of the preventative roles of manganese superoxide dismutase Ala16Val gene polymorphism in coronary artery events

Amaç: Araştırmamızın amacı, mangan süperoksit dismutaz (MnSOD) genine ait Ala16Val polimorfizminin koroner arter hastalığı (KAH) olan kişilerdeki genotip sıklıklarını belirlemek ve genotip-kalp damar hastalığı ve genotip-biyokimyasal parametreler ve serum MnSOD aktivitesi ile etkileşimin değerlendirilmesidir. Gereç ve yöntemler: MnSOD geni Ala16Val genotipleri kantitatif polimeraz zincir reaksiyonu yöntemi ile saptandı. Serum MnSOD aktivitesi ELİSA yöntemi ile belirlendi. Bulgular: MnSOD geni Ala16Val polimorfizmi için genotip sıklıkları KAH grubunda C/C (Homozigot yabanıl tip), C/T (Heterozigot), T/T (Homozigot polimorfik tip) genotipler için sırasıyla %20.9, %41.9, %37.2 ve KAH olmayan grupta %15.5, %51.7, %32.8 olarak tespit edildi. Tüm çalışma grubundaki mitokondriyal MnSOD aktiviteleri, MnSOD geni Ala16Val genotiplerine göre karşılaştırıldığında CC genotip taşıyıcılarının en yüksek, TT genotip taşıyıcılarının en düşük MnSOD aktivitesine sahip olduğu belirlendi. Koroner arter hastalığı bulunmayan hastalarda MnSOD Ala16Val polimorfizminin yağsız vücut kütlesi (p=0.01) ve yağ kütlesi (p=0.05) üzerine anlamlı etkileri olduğu saptandı. Ala16Val polimorfizminin heterozigot genotipe sahip KAH hastalarında yağdan zengin gıdalarla beslenme alışkanlıkları diğer genotiplere kıyasla daha düşük iken, homozigot polimorfik genotipe sahip KAH hastalarının diğer genotiplere kıyasla proteinden fakir beslenme alışkanlıklarını benimsedikleri görüldü. Sonuç: Tüm çalışma grubu değerlendirildiğinde, MnSOD Ala16Val genotipleri ile beslenme alışkanlıkları arasında anlamlı bir ilişki bulunurken yağsız vücut kütlesi üzerinde etkili bulunmamıştır.Objectives: The aim of this study was to determine the genotypic frequencies of manganese superoxide dismutase (MnSOD) gene Ala16Val polymorphism frequencies and to evaluate the effects of MnSOD Ala16Val variation over coronary artery disease (CAD) in which people, biochemical parameters and MnSOD activity. Materials and methods: MnSOD gene Ala16Val polymorphisms were determined with quantitative polymerase chain reaction method. MnSOD activity in serum were determined by ELISA method. Results: The MnSOD gene Ala16Val genotype frequencies were determined respectively as 20.9%, 41.9%, 37.2% for homozygous wild genotype (C/C), heterozygous genotypes (C/T), homozygous polymorphic genotype (T/T) in the CAD patients; whereas 15.5%, 51.7% and 32.8% for the patients without CAD. In total study group, C/C genotype carriers were detected to have the highest, whereas T/T genotype carriers were detected to have the lowest mitochondrial MnSOD activities when compared according to MnSOD gene Ala16Val genotypes. In the patients without CAD, MnSOD Ala16Val polymorphism was found to have significant effects on lean body mass (p=0.01) and fat mass (p=0.05). In CAD patients with Ala16Val polymorphism heterozygous genotype oil-rich eating habits were lower to that of other genotypes, whereas CAD patients with homozygous polymorphic genotype was detected to prefer protein-poor diet. Conclusion: When all the study group was evaluated, MnSOD Ala16Val genotypes were not found to have statistically significant relationship with eating habits, but found to be effective only on lean body mass

Omentum adiposity is linked with resistin gene expression

Background: This study demonstrated site-specific adipose tissue resistin gene expression differences in individuals with and without type 2 diabetes mellitus. The relationship between conventional drug therapy and adipose tissue resistin gene expression was also determined. Paired omental and subcutaneous adipose tissues were excised during elective surgery from morbidly obese and obese patients. Methods: Resistin mRNA expressions were determined by qPCR. All tissue sections also were also analyzed for their resistin and CD68 protein expressions by immunohistochemistry. Results: No significant difference for omental and subcutaneous adipose tissue resistin mRNA expression levels were found among morbidly obese and obese study groups. The omental adipocytes resistin mRNA expressions increased with macrophage number both in the omental and subcutaneus fat. Resistin mRNA expressions of the omental and subcutaneous fat were in positive correlation. As the omental adipocytes radius decreased, the macrophage number increased in subcutaneous fat. In the omentum the adipocytes diameter and areas increased, in correlation with macrophage number. The antidiabetic drug use was found to increase adipocyte size both in the omentum and subcutaneous fat. Conclusions: The higher resistin gene expression in the omental fat may induce the increase in size and number of adipocytes, thus leading to elavation in omental fat mass