In Fig-1 shown that, in the primary phase of glycosylated hemoglobin formation, hemoglobin and blood glucose react reversibly to the aldimine. In the irreversible secondary phase, aldimina gradually becomes a stable 6 form of ketoamine. The main sites of hemoglobin glycosylation are in the order of their prevalence β-Val-1, β-Lys-66 and α-Lis-61. Normal adult hemoglobin
Cardiac hypertrophy (CH) is an augmentation of either the right ventricular or the left ventricular mass in order to compensate for the increase of work load on the heart. Metabolic abnormalities lead to histological changes of cardiac myocytes and turn into CH. The molecular mechanisms that lead to initiate CH have been of widespread concern, hence the development of the new field of research, metabolomics: one ‘omics’ approach that can reveal comprehensive information of the paradigm shift of metabolic pathways network in contrast to individual enzymatic reaction-based metabolites, have attempted and until now only 19 studies have been conducted using experimental animal and human specimens. Nuclear magnetic resonance spectroscopy and mass spectrometry-based metabolomics studies have found that CH is a metabolic disease and is mainly linked to the harmonic imbalance of glycolysis, citric acid cycle, amino acids and lipid metabolism. The current review will summarise the main outcomes of the above mentioned 19 studies that have expanded our understanding of the molecular mechanisms that may lead to CH and eventually to heart failure.
Background: Endothelial nitric oxide synthase (eNOS) and potassium voltage-gated channel subfamily J member 11 (KCNJ11) could be the candidate genes for coronary artery disease (CAD). This study investigated the relationship of the eNOS (rs1799983) and KCNJ11 (rs5219) polymorphisms with the presence and severity of CAD in the North Indian pop- ulation.
Methods: This study included 300 subjects, 150 CAD cases and 150 healthy controls. Single nucleotide polymorphism was evaluated by Polymerase chain reaction and Restriction fragment length polymorphism (PCR-RFLP). Analysis was performed by SPSS (version 21.0).
Results: We observed that KK genotype of KCNJ11E23K (rs5219) polymorphism (P=0.0001) genotypes and K allele (P=0.0001) was found to be a positive risk factor and strongly associated with CAD. In the case of eNOSG894T (rs1799983) there was no association found with CAD.
Conclusion: These results illustrate the probability of associations between SNPs and CAD although specific genetic pol- ymorphisms affecting ion channel function and expression have still to be clarified by further investigations involving larger cohorts.
Keywords: Coronary Artery Disease (CAD); endothelial nitric oxide synthase (eNOS); potassium voltage-gated channel subfamily J member 11 (KCNJ11); gene polymorphism.
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