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Predisposition to diabetes is attributed to a large number of genes. TCF7L2 is one of the most significant candidate genes among them, and it is crucial for beta-cell activity and blood glucose regulation. According to previous research, TCF7L2 has been implicated in T2DM in various Indian tribes. Many studies have discovered a link between TCF7L2 gene variations and vulnerability to T2DM. These results suggest that changes in TCF7L2 expression are not only associated with insulin resistance but also with risk for genotypes connected to poor beta cell activity. TCF7L2 drives the conventional Wnt signalling pathway and functions as a nuclear ligand for beta catenin. Wnt signalling is necessary for intestinal endocrine L-cells to emit GLP-1 (glucagon-like peptide-1). As a result, a blockage in this route would cause less GLP-1 to be released, which might have an impact on the release of insulin after meals contributing to T2DM as a result. The molecular processes through which the TCF7L2 gene increases the susceptibility of T2DM will therefore be of significant interest, as will the identification of possible therapeutic targets that may be employed to treat and prevent the illness as a result of the gene variations.

T-cadherin, a special member of cadherin family, expresses with blood circulation involving the heart i.e. CVS. Cadherin is connected with the healthy conditions of an individual and normal functioning of cardio-vascular metabolism. T-cadherin is mainly associated with blood vascular system of human. Previous studies analysed this cadherin been unexpressed within the fat storing tissues i.e. adipose tissue of peri-aortic and peri-coronary, it is present within endothelium as well as in vascularized smooth muscular cells which includes the area nearby coronary vessels and aorta. The area and site of this cadherin is attention-grabbing because it particularly related to atherosclerosis and cardiovascular disease (CVD). T-cadherin - a protein acting as the receptor for low density lipoproteins (LDL). It may act as a special biomarker for atherosclerosis. Previous studies on T-cadherin showed that it has cardio-protective role. Furthermore, research is essential to enumerate the cardio-protective function of T-cadherin. It can be an important therapeutic target in developing new medicine to decrease incident of heart disease and its complications.

Introduction: Microalbuminuria has recently emerged as an early marker of hypertension induced target organ damage. Microalbuminuria in hypertensive patients may act as a potential risk factor for cardiovascular and kidney diseases. Objective:The aim of the study is to evaluate the levels of microalbuminuria in hypertensive (HT) patients and normotensive (NT) control subjects. Materials and Methods:In this case-control study, 42 HT patients and 42 age and gender matched NT controls were enrolled. Body mass index (BMI), systolic and diastolic blood pressure (SBP and DBP) was measured by standard protocol. Urinary microalbumin and creatinine were estimated in spot urine sample of all subjects using commercially available kit. Chi-square test, unpaired t test and Pearson correlation coefficient were used for Statistical analysis. The p-value Results:In this study, results showed that more than half of the HT patients have smoking habits (59.3%), alcoholic habits (71.4%) and family history of HT (73.8%), which is significantly higher as compared to NT controls (p=0.02, p=0.004, p=0.02, respectively). Anthropometric parameters height, weight and BMI were found significantly higher in HT patients as compared to NT controls (p=0.01, p=0.007, p=0.001, respectively). Mean of SBP and DBP were also found significantly higher in HT patients than NT controls (p=0.001, p=0.001, respectively). Urinary microalbumin, urinary creatinine and albumin creatinine ratio (ACR) were found significantly higher in HT patients as compared to NT controls (p=0.02, p=0.01, p=0.02, respectively). Correlation of various anthropometric and clinical parameters showed that ACR have significantly positive correlation with age in HT patients (r=0.364, pnegative correlation with age in HT patients, but not significant (r= -0.027). Similarly, ACR also have negative correlation with BMI, SBP and DBP in HT patients (r= -0.068, r= -0.145, r= -0.219, respectively), but these are not significant. Conc

Various adiponectin gene (ADIPOQ) variants, located on chromosome 3q27 were associated with Type 2 diabetes mellitus (T2DM) in different ethnicity.In this study, it is aimed to find the association of +10211T/G (rs17846866) variant of ADIPOQ with T2DM and healthy controls in North Indians.In this study, 150 T2DM and 150 healthy control subjects aged between 25-75 years were recruited. Circulatory adiponectin levels were measured by commercially available ELISA kit. For genotype analysis, Polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) method was used.The genotypic analysis of rs17846866 variant of ADIPOQ has shown that there were no significant association of TT versus TG genotype (P=0.13) as well as TT versus GG genotype (P=0.11) with T2DM patients and healthy controls. However, the G allele frequency of the rs17846866 has shown significant association with T2DM (13.7%) as compared to healthy controls (7.7%, P=0.02). In T2DM, circulatory adiponectin level was significantly lower in TT genotype than TG genotypes (P=0.01). However, the circulatory adiponectin level was lower in GG genotype than TG genotype (P=0.49), but not significant.The result showed that rs17846866 variant of ADIPOQ was associated with altered circulatory adiponectin levels. The TT genotype may be the major contributor to reduce the circulatory adiponectin levels in T2DM. However, the G allele may be increased the risk of T2DM in North Indians.

Diabetic nephropathy (DN) is a chronic complication of both type 1 and type 2 diabetes. However, there is still inadequate understanding of the exact mechanism related to progressive diabetic renal disease. The GLUT-1 XbaI gene polymorphism in the glucose transporter has been suggested in the development of DN. However, its association with T2DM and DN is controversial and has not been established in different ethnic populations. To enhance the understanding of GLUT-1 XbaI gene polymorphism in the context of T2DM and DN. We investigated the possible genetic association of GLUT-1 XbaI polymorphism with T2DM and DN in North Indian population. 100 T2DM patients and 100 patients of DN with 100 healthy controls were included in the study. GLUT-1 XbaI polymorphism was determined by PCR (polymerase chain reaction) and RFLP (restriction fragment length polymorphism). The obtained data showed no significant association between GLUT-1 XbaI gene polymorphism with T2DM and DN leading us to conclude that GLUT-1 XbaI gene polymorphism may not have major effects on T2DM and DN in North Indian population.

Background: The incidence and prevalence of type 2 diabetes mellitus (T2DM) is increasing due to obesity and sedentary lifestyles. Increased oxidative stress leads to oxidative damage of biomolecules and decreased antioxidant capacity.Aim: The study was designed to determine the malondialdehyde (MDA) and ferric reducing ability of plasma (FRAP) in T2DM patients at IIMS&R Hospital, Lucknow.Method: The oxidative stress was analyzed in T2DM patients as MDA. The total antioxidant capacity was estimated through the FRAP in T2DM patients and control subjects.Results: The level of MDA was observed to be higher (4.84 ± 1.09) in T2DM patients compared to controls (2.20 ± 0.85). The FRAP was lower among T2DM patients (509.46 ± 126.36) compared to controls (895.62 ± 179.92). The difference between FRAP in T2DM patients and controls was statistically significant (p=0.0001).Conclusion: MDA was found to be higher in T2DM, and the FRAP level was lower in T2DM patients compared to controls, signifying increased oxidative stress and decreased antioxidant level in T2DM patients.

Metabolism is a delicately coordinated entity of chemical reactions. Inborn Errors of Metabolism (IEM) are rare congenital disorders that are mainly due to gene defect of enzymes or cofactors participating in a metabolic pathway or the transport of metabolites within a cell or between cells. The development of knowledge in basic sciences together with technology development in medical field has helped to better understand the molecular and biochemical basis of IEM. Environmental factors, ethnicity, race, consanguinity and genetic factors contribute to the increased prevalence of genetic disorders. The analytical methods have evolved over the years from thin layer chromatography (TLC), high performance liquid chromatography (HPLC) to tandem mass spectrometry (TMS) including gas chromatography mass spectrometry (GC/MS). Their applications for È¡7_Ø‹5_g of IEM has opened the door for screening of conditions that previously required molecular testing or another methodology that was not practical for population-based screening. Future technologies such as Matrix-assisted laser desorption/ ionization timeof- flight mass spectrometry (MALDI-TOF MS), has the potential for rapid and reliable identification of small metabolites and disease biomarkers in daily clinical laboratories, whereas DNA based screening by DNA microarrays or gene chips will allow much more improved diagnosis.These can be the boon to screening programs which will require excellent detection and follow-up servicesInternational Journal of Human and Health Sciences Vol. 03 No. 02 April’19. Page: 58-63

The present study was designed to probe the possible role of singlet oxygen and superoxide anion radical modified DNA in the etiopathogenesis of Systemic lupus erythematosus. These species were generated by the exposure of riboflavin to 365 nm UV light. Modified DNA showed single strand breaks, hyperchromicity at 260nm and decrease in Tm. The modified DNA induced high titer antibodies in experimental animals. The antibodies showed reactivity with various nucleic acid polymers, a property commonly associated with Systemic lupus erythematosus anti-DNA autoantibodies. Systemic lupus erythematosus sera showed preferential binding of modified DNA over native DNA in direct binding and competitive binding solid phase immunoassays and band shift assays. The results suggest for the possible involvement of the singlet- superoxide modified DNA as a potential trigger for anti- DNA autoantibody production in SLE and thus in the etiopathogenesis of the disease.