Cardiac metabolism supplies the heart with the ATP required to maintain its energy-consuming pumping function. At the molecular level, the heart's metabolism is governed by biochemical reactions enabling the utilization of various fuel sources to generate adenosine triphosphate (ATP). The heart's ability to adapt its metabolic pathways to changing energy demands is essential for its normal functioning and responses to different physiological and pathological conditions. The heart predominantly utilizes three main substrates for energy production: fatty acids, glucose, and to a lesser extent, ketone bodies. These substrates are metabolized through interconnected pathways that involve several key enzymes and regulators. Fatty acids are the heart's primary energy source. During fatty acid oxidation (FAO), long-chain fatty acids are metabolized in mitochondria through a series of enzymatic reactions, including beta-oxidation. This process generates acetyl-CoA, which enters the citric acid cycle (TCA cycle) to produce reducing equivalents in the form of NADH and FADH2. Glucose can be metabolized in the heart through two main pathways: glycolysis and oxidative phosphorylation. Glycolysis converts glucose to pyruvate, generating ATP and NADH. Pyruvate can then enter the mitochondria, where it is converted to acetyl-CoA and enters the citric acid cycle. Alternatively, glucose can be metabolized through the pentose phosphate pathway to generate reducing equivalents and ribose for nucleotide synthesis. During periods of fasting or ketogenic diets, the heart can also utilize ketone bodies—acetoacetate and beta-hydroxybutyrate—as an energy source. Ketone bodies are also subsequently converted to acetyl-CoA and enter the citric acid cycle.The heart's metabolism is highly adaptive, allowing it to respond to changes in energy demands. This adaptability is controlled by various molecular regulators. Firstly, the hormones insulin and glucagon play critical roles in regulating substrate utilization. Insulin promotes glucose uptake and utilization, whilst glucagon stimulates fatty acid oxidation and ketone body production during periods of low glucose availability. AMPK is a cellular energy sensor that becomes activated when the cellular AMP/ATP ratio is elevated. AMPK in the heart stimulates pathways that enhance energy production, such as fatty acid oxidation and glucose uptake, whilst inhibiting energy-consuming processes. Peroxisome Proliferator-Activated Receptors (PPARs) are nuclear receptors that regulate gene expression related to fatty acid oxidation and glucose metabolism. PPARs coordinate the utilization of different substrates based on the heart's energy needs. Finally, Hypoxia-Inducible Factor-1 (HIF-1) is activated in the heart in response to low oxygen levels (hypoxia) and can influence glucose metabolism, glycolysis, and lactate production to support energy production under oxygen-deficient conditions. The heart's metabolic flexibility is essential for maintaining contractile function, especially during periods of increased demand, such as exercise or stress. Dysregulation of cardiac metabolism is associated with various cardiovascular diseases, including heart failure, diabetes, and ischemic heart disease. Shifts in substrate utilization and alterations in metabolic pathways can impair ATP production, contractile function, and overall cardiac health. We provide a large product range of research tools for investigating cardiac metabolism, including Catalase antibodies, Creatine Kinase MB antibodies, SIRT3 antibodies, Catalase ELISA Kits, and pan-AKT ELISA Kits. Explore our full cardiac metabolism product range below and discover more, for less.