Myocardial infarction is a major cause of deaths globally. Modulation of several molecular mechanisms occurs during the initial stages of myocardial ischemia prior to permanent cardiac tissue damage, which involves both pathogenic as well as survival pathways in the cardiomyocyte. Currently, there is increasing evidence regarding the cardioprotective role of vitamin E in alleviating the disease. This fat-soluble vitamin does not only act as a powerful antioxidant; but it also has the ability to regulate several intracellular signalling pathways including HIF-1, PPAR-γ, Nrf-2, and NF-κB that influence the expression of a number of genes and their protein products. Essentially, it inhibits the molecular progression of tissue damage and preserves myocardial tissue viability. This review aims to summarize the molecular understanding of the cardiomodulation in myocardial infarction as well as the mechanism of vitamin E protection.
Metabolic syndrome (MetS) is a group of conditions including central obesity, hyperglycemia, dyslipidemia, and hypertension that increases the risk for cardiometabolic diseases. Kelulut honey (KH) produced by stingless honey bees has stronger antioxidant properties compared to other honey types and may be a functional food against MetS. This study aimed to determine the efficacy of KH in preventing metabolic changes in rats with MetS induced by high-carbohydrate and high-fat (HCHF) diet. Male Wistar rats were randomly assigned to the control (C), HCHF diet-induced MetS (S), and MetS supplemented with KH (K) groups. The K group was given KH (1 g/kg/day) for eight weeks. Compared to the control, the S group had significant higher omental fat mass, serum triglyceride, systolic blood pressure, diastolic blood pressures, adipocyte area, and adipocyte perimeter (p < 0.05). KH supplementation significantly prevented these MetS-induced changes at week 16 (p < 0.05). Several compounds, including 4-hydroxyphenyl acetic acid, coumaric and caffeic acids, had been detected via liquid chromatography-mass spectrometry analysis that might contribute to the reversal of these changes. The beneficial effects of KH against MetS-induced rats provide the basis for future KH research to investigate its potential use in humans and its molecular mechanisms in alleviating the disease.
Metabolic syndrome (MetS) is a cluster of diseases comprising of obesity, diabetes mellitus, dyslipidemia, and hypertension. There are numerous pre-clinical as well as human studies reporting the protective effects of honey against MetS. Honey is a nutritional food low in glycemic index. Honey intake reduces blood sugar levels and prevents excessive weight gain. It also improves lipid metabolism by reducing total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL) and increasing high-density lipoprotein (HDL), which leads to decreased risk of atherogenesis. In addition, honey enhances insulin sensitivity that further stabilizes blood glucose levels and protects the pancreas from overstimulation brought on by insulin resistance. Furthermore, antioxidative properties of honey help in reducing oxidative stress, which is one of the central mechanisms in MetS. Lastly, honey protects the vasculature from endothelial dysfunction and remodelling. Therefore, there is a strong potential for honey supplementation to be integrated into the management of MetS, both as preventive as well as adjunct therapeutic agents.
Malaysia has high prevalence of general and central obesity which can be signified by measurements of BMI and waist circumference respectively. Both parameters are established risk factors and predictors for non-communicable diseases including diabetes and hypertension. A health screening programme was conducted in a rural district of Sabah, Malaysia where a total of 42 participants were examined for weight, height, BMI, waist circumference, systolic and diastolic blood pressure, pulse rate and capillary blood glucose. Mean age of the participants was 52.4 ± 14.9 years old. General obesity based on BMI was 42.9% while central obesity based on waist circumference was 26.2%. Proportion for hypertension and hyperglycaemia were equal at 33.3%. BMI was strongly correlated to waist circumference (r = 0.873, p < 0.001). Moreover, both BMI and waist circumference were independently correlated with systolic blood pressure (r = 0.418, p = 0.006 and r = 0.383, p = 0.012 respectively). Finally, systolic blood pressure was directly correlated with weight of the participants (r = 0.350, p = 0.023). These findings were found to be closely similar and comparable to currently available epidemiological data.
Genome-wide association studies (GWAS) have discovered 163 loci related to coronary heart disease (CHD). Most GWAS have emphasized pathways related to single-nucleotide polymorphisms (SNPs) that reached genome-wide significance in their reports, while identification of CHD pathways based on the combination of all published GWAS involving various ethnicities has yet to be performed. We conducted a systematic search for articles with comprehensive GWAS data in the GWAS Catalog and PubMed, followed by a meta-analysis of the top recurring SNPs from ≥2 different articles using random or fixed-effect models according to Cochran Q and I2 statistics, and pathway enrichment analysis. Meta-analyses showed significance for 265 of 309 recurring SNPs. Enrichment analysis returned 107 significant pathways, including lipoprotein and lipid metabolisms (rs7412, rs6511720, rs11591147, rs1412444, rs11172113, rs11057830, rs4299376), atherogenesis (rs7500448, rs6504218, rs3918226, rs7623687), shared cardiovascular pathways (rs72689147, rs1800449, rs7568458), diabetes-related pathways (rs200787930, rs12146487, rs6129767), hepatitis C virus infection/hepatocellular carcinoma (rs73045269/rs8108632, rs56062135, rs188378669, rs4845625, rs11838776), and miR-29b-3p pathways (rs116843064, rs11617955, rs146092501, rs11838776, rs73045269/rs8108632). In this meta-analysis, the identification of various genetic factors and their associated pathways associated with CHD denotes the complexity of the disease. This provides an opportunity for the future development of novel CHD genetic risk scores relevant to personalized and precision medicine.