Background/Objectives: The global high prevalence of cardiovascular diseases (CVDs) is attributed to the high prevalence of obesity and metabolic syndrome. However, the impact of a high-fat diet (HFD) on the expression of genes in cardiac tissue remains poorly understood. Methods: A thorough literature search was performed using PubMed, Scopus, EBSCOhost, and ScienceDirect databases. The Medical Subject Heading (MeSH) terms such as “high-fat diet”, “gene expression” and “cardiac tissue” were used as the keywords in all fields. Results: A total of 1608 studies were retrieved, and only in vivo experimental studies to identify cardiac tissues differentially expressed genes (DEGs) or proteins (DEPs) in rodents fed with HFD were selected. After screening, 14 studies were selected, 159 DEGs and DEPs were extracted from the data and further analysis was conducted employing DAVID, STRING, and Cytoscape 3.10.3 software. A protein–protein interaction (PPI) network revealed a total of 159 genes and proteins from the selected DEGs containing 100 nodes and 292 edges with a PPI enrichment p-value of < 1.0 × 10⁻¹⁶ and an average local clustering coefficient of 0.447 with an average node degree of 5.84. Six significant clusters with high intermolecular interactions from the protein–protein interaction (PPI) network complex reveal significant molecular pathways, including the glucose metabolic process, fatty acid metabolic process, and inflammatory response (p < 0.05). Conclusions: The identification of the critical link between obesity and HFD-induced CVDs in cardiac tissue highlights the need for a deeper understanding of the molecular mechanisms controlling gene expression in cardiac tissue.

Background: Non-alcoholic fatty liver disease (NAFLD) has been associated with metabolic syndrome (MetS). One of the underlying mechanisms of NAFLD is an aberration in amino acid metabolism and signalling. The tocotrienol-rich fraction (TRF) has been shown to improve NAFLD and is thus recommended as a supplement in NAFLD. However, TRF often exhibits low bioavailability. Recently, our group reported that TRF with medium-chain triglyceride (MCT) carriers could potentially improve steatosis, bile acid metabolism, lipid, and fatty acid metabolism. Objective: This study investigated the effects of TRF-MCT on amino acid metabolism in an NAFLD mice model. Methods: Male B6.Cg-LepOb/J mice were used as an NAFLD mouse model and randomly divided into three groups: high-fat diet only (HFD), TRF-MCT, and palm kernel oil (PKO) (vehicle MCT). After 6 weeks of supplementation, serum was collected for untargeted metabolomic analysis using ultrahigh-performance liquid chromatography-mass spectrometry (UHPLC-MS), significant metabolic features were annotated to determine the fold change (FC), and analysis was performed (SIMCA and MetaboAnalyst). Results: In the TRF-MCT group, 11 amino acids were annotated. Urocanic acid group (FC = 1.0146), ascorbic acid 2-sulphate (FC = 0.81939), 3-isoproprylmalic acid (FC = 0.66469), and 6-methylnicotamide (FC = 0.6507) were the most upregulated (p < 0.05). Lysine (FC = − 0.88836), leucine (FC = − 0.7949), pyridoxamine (FC = − 0.76347), 3-indoxyl sulphate (FC = − 0.73989), threonine (FC = − 0.66945), and indolelactic acid (FC = − 0.61605) were the most downregulated (p < 0.05). Glutamic acid (FC = 0.79069) levels were upregulated in the PKO-treated group compared to the HFD group (p < 0.05). Conclusion: TRF-MCT-supplemented NAFLD mouse model shown an altered amino acid which involves in valine, leucine, and isoleucine biosynthesis, aminoacyl-transfer RNA (aminoacyl-tRNA) biosynthesis, and vitamin B6 metabolism. Thus, suggesting TRF-MCT has a protective effect and repairing activities in the liver of the NAFLD mouse model.