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In Pakistan and other developing countries, the available data on the association of T2DM and HCV is limited. We therefore made an attempt to report the association of HCV and diabetes in Pakistani population through this meta-analysis. HCV and diabetes related studies were identified using various key words, from a number of databases including CINAHL, PubMed, Web of Science and Embase. Using RevMan5, the main outcome was regarded as type 2 diabetes associations with hepatitis c virus infection in Pakistan. Independent analyses were made for "HCV in diabetic patients" and "diabetes cases in hepatitis C virus patients". Using random effect model, odds ratios were calculated with 95% CIs (dichotomous data). I2 statistics were used to calculate heterogeneity. From a total of 53 studies, we finally selected 6 studies for the meta-analysis. Using random effects model, hepatitis c virus patients in 3 studies (n = 1,902) demonstrated that HCV is a risk factor in developing diabetes, contrary to patients with no HCV infection (OR 0.01, 95% CI: 0.00-0.06, I2 = 0%; RR 0.01, 95% CI: 0.00-0.07, I2 = 0%). The remaining 3 studies (n = 13,710) had reported HCV infections in type 2 diabetic patients and patients with no diabetes. Similarly, our meta-analysis revealed higher prevalence of HCV infections in patients with type 2 diabetes (OR 0.7, 95% CI: 0.17-0.42, I2 = 32%; RR 0.30, 95% CI: 0.20-0.46, I2 = 32%) as compared to patients with no type 2 diabetes mellitus. Our meta-analysis demonstrates a significant link between HCV and T2DM. Further studies are recommended with adequate sample sizes [ABSTRACT FROM AUTHOR]

Objective: The objective was to study the association of Klotho gene G395A and C1818T single nucleotide polymorphisms with glycemia, serum, glycosylated hemoglobin (HbA1c) level and the risk of type 2 diabetes mellitus (T2DM) in the Pashtun population of Pakistan. Methods: In this study, 195 normal individuals and 217 T2DM patients were enrolled. All subjects were divided into three groups, namely overall subjects (control + T2DM patients), control individuals and T2DM patients, and their fasting glucose, HbA1c level, lipid profile and C1818T and G395A polymorphisms were determined. Results: The allele frequencies of G395A in overall subjects were 0.568 for A and 0.432 for G. Similarly, allele frequencies for G395A in overall subjects were 0.597 and 0.403 for C and T alleles, respectively. The AA genotype of G395A was observed to be a risk factor for T2DM. In normal individuals, no significant (p > 0.05) association was observed between klotho C1818T and G395A polymorphisms and hyperglycemia. In overall subjects, the C1818T polymorphism was associated (p < 0.05) with high fasting glucose and HbA1c levels in female subjects only. In T2DM patients, both C1818T and G395A polymorphisms were found to be significantly (p < 0.05) associated with high fasting glucose and HbA1c levels both in males and females. Conclusion: The G395A polymorphism was observed to increase the risk of T2DM. Both C1818T and G395 were associated with high fasting glucose and HbA1c levels in T2DM patients. [ABSTRACT FROM AUTHOR]

Background/Aims: NF-κB induces transcription of a number of genes, associated with inflammation and apoptosis. In this study, we have investigated the effect of β-adrenergic receptor stimulation on NF-κB and IκBα in HUVECs. Methods: Human umbilical vein endothelial cells (HUVECs) were cultured in high and low glucose concentrations. All HUVECs were treated with different concentrations of isoproterenol and propranolol for different time periods. The analytical procedures consisted of Western Blot, ELISA, DCFH-DA and TUNEL assays. Results: Isoproterenol (agonist of a beta-adrenergic receptor) significantly reduced phosphorylation at Ser-536 of NF-κB; and Ser-32 and Ser-36 of IκBα in hyperglycemic HUVECs. Isoproterenol also significantly reduced apoptosis and ROS generation. No effect of IκBα was observed on Tyr-42 phosphorylation. The effect of isoproterenol was reversed by the antagonist propranolol. We also checked if NF-κB inhibitor MG132 causes any change at the level of apoptosis. However, we observed an almost similar effect. Conclusion: Given data demonstrates that beta-adrenergic receptors stimulation has a protective effect on HUVECs that might be occuring via NF-κβ and IκBα pathway. [ABSTRACT FROM AUTHOR]