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.

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.

Asians are more susceptible to type 2 diabetes mellitus (T2D) and its coronary heart disease (CHD) complications than the Western populations, possibly due to genetic factors, higher degrees of obesity, insulin resistance, and endothelial dysfunction that could occur even in healthy individuals. The genetic factors and their mechanisms, along with gene-gene and gene-environment interactions associated with CHD in T2D Asians, are yet to be explored. Therefore, the objectives of this paper were to review the current evidence of genetic factors for CHD, summarize the proposed mechanisms of these genes and how they may associate with CHD risk, and review the gene-gene and gene-environment interactions in T2D Asians with CHD. The genetic factors can be grouped according to their involvement in the energy and lipoprotein metabolism, vascular and endothelial pathology, antioxidation, cell cycle regulation, DNA damage repair, hormonal regulation of glucose metabolism, as well as cytoskeletal function and intracellular transport. Meanwhile, interactions between single nucleotide polymorphisms (SNPs) from different genes, SNPs within a single gene, and genetic interaction with environmental factors including obesity, smoking habit, and hyperlipidemia could modify the gene’s effect on the disease risk. Collectively, these factors illustrate the complexities of CHD in T2D, specifically among Asians.

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.

: 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.

Purpose: To determine the effects of Kelulut honey (KH) on the bone health of rats with metabolic syndrome. Methods: Male Wistar rats were randomised into normal control and metabolic syndrome is fed with a diet enriched with carbohydrate and fat. The rats in the metabolic syndrome arm were further assigned into the negative control group and honey group supplemented orally with Kelulut honey (1g/kg) daily for eight weeks. After the rats were sacrificed, the trabecular and cortical micro-architecture of the harvested femur was analysed using X-ray micro-computed tomography, while histomorphometric method was used to determine bone cell indices. Femoral biomechanical properties were analysed using a universal mechanical tester. Results: Total cross-sectional area, osteoid surface and volume, displacement and strain reduced significantly, while eroded surface increased significantly in the rats with metabolic syndrome than the normal rats (p < 0.05). The honey group showed a significant reduction in osteoclast surface than the normal healthy control (p < 0.05). Other skeletal parameters did not show a significant intergroup difference. Conclusion: Metabolic syndrome is harmful to bone health and honey has limited effects in reversing these negative effects.