What is the direct product of triglyceride hydrolysis in adipose tissue that is then oxidized for energy, assuming a caloric deficit?

The direct products of triglyceride hydrolysis in adipose tissue that are subsequently oxidized for energy are glycerol and fatty acids. Triglycerides, the primary form of stored energy in adipose tissue, are molecules composed of a glycerol backbone esterified to three fatty acid chains. During hydrolysis, a chemical reaction involving water that breaks chemical bonds, these ester bonds are broken by enzymes called lipases. This process, stimulated by hormones such as glucagon and epinephrine in a caloric deficit (when energy intake is less than energy expenditure), releases free glycerol and three free fatty acid molecules from the stored triglyceride. These products are then mobilized for energy production. Glycerol, a three-carbon alcohol, is released into the bloodstream and primarily transported to the liver. In the liver, glycerol is phosphorylated, meaning a phosphate group is added, by the enzyme glycerol kinase to form glycerol-3-phosphate. Glycerol-3-phosphate is then oxidized by glycerol-3-phosphate dehydrogenase to dihydroxyacetone phosphate (DHAP). DHAP is a metabolic intermediate that can enter the gluconeogenic pathway, which is the process of synthesizing glucose from non-carbohydrate precursors, or directly enter the glycolytic pathway, which is the breakdown of glucose. Ultimately, the carbons from glycerol are further metabolized through the citric acid cycle (also known as the Krebs cycle) and oxidative phosphorylation, where they are completely oxidized to carbon dioxide and water, generating ATP, the cell's main energy currency. Fatty acids, which are long hydrocarbon chains, are also released into the bloodstream from adipose tissue and bind to albumin for transport to various tissues, including muscle and liver, for energy production. Upon entering target cells, fatty acids are activated in the cytoplasm, the jelly-like substance filling a cell, by attaching to Coenzyme A (CoA) to form fatty acyl-CoA, a process that requires ATP. Long-chain fatty acyl-CoA molecules are then transported into the mitochondrial matrix, the inner compartment of the mitochondria where cellular respiration occurs, via the carnitine shuttle system. Inside the mitochondrial matrix, fatty acids undergo beta-oxidation. Beta-oxidation is a cyclical metabolic pathway that sequentially removes two-carbon units from the fatty acyl-CoA chain, releasing them as acetyl-CoA. Each cycle of beta-oxidation also produces one molecule of FADH2 and one molecule of NADH, which are electron carriers. The acetyl-CoA molecules then enter the citric acid cycle, where they are completely oxidized to carbon dioxide, generating more NADH and FADH2. The NADH and FADH2 produced from both beta-oxidation and the citric acid cycle donate electrons to the electron transport chain, a series of protein complexes located in the inner mitochondrial membrane, driving oxidative phosphorylation. Oxidative phosphorylation is the primary mechanism for synthesizing a large amount of ATP by using the energy released from the transfer of electrons, ultimately producing water. Thus, both direct products of triglyceride hydrolysis, glycerol and fatty acids, are extensively oxidized to generate cellular energy in a caloric deficit.