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Therefore, ketone bodies are a way to move energy from the liver to other cells. The liver does not have the critical enzyme, succinyl CoA transferase, to process ketone bodies, and therefore cannot undergo ketolysis. [6] [11] The result is that the liver only produces ketone bodies, but does not use a significant amount of them. [16]
Ketone bodies are water-soluble molecules or compounds that contain the ketone groups produced from fatty acids by the liver (ketogenesis). [1] [2] Ketone bodies are readily transported into tissues outside the liver, where they are converted into acetyl-CoA (acetyl-Coenzyme A) – which then enters the citric acid cycle (Krebs cycle) and is oxidized for energy.
The ketone bodies are possibly anticonvulsant; in animal models, acetoacetate and acetone protect against seizures. The ketogenic diet results in adaptive changes to brain energy metabolism that increase the energy reserves; ketone bodies are a more efficient fuel than glucose, and the number of mitochondria is increased.
The resulting ketone bodies cannot be used for energy by the liver so are exported from the liver to supply energy to the brain and peripheral tissues. In addition to fatty acids, deaminated ketogenic amino acids can also be converted into intermediates in the citric acid cycle and produce ketone bodies. [11]
This class of ketone bodies refers to the three water-soluble ketones (acetoacetate, β-hydroxybutyrate [β-HB], and acetone). [1] These ketone bodies are produced by interactions between macronutrient availability such as low glucose and high free fatty acids or hormone signaling such as low insulin and high glucagon/cortisol. [2]
Thus, the production of ketone bodies cuts the brain's glucose requirement from 80 g per day to about 30 g per day. Of the remaining 30 g requirement, 20 g per day can be produced by the liver from glycerol (itself a product of fat breakdown). This still leaves a deficit of about 10 g of glucose per day that must come from some other source.
A ketogenic amino acid is an amino acid that can be degraded directly into acetyl-CoA, which is the precursor of ketone bodies and myelin, particularly during early childhood, when the developing brain requires high rates of myelin synthesis. [1] This is in contrast to the glucogenic amino acids, which are converted into glucose.
DKA results from a shortage of insulin; in response, the body switches to burning fatty acids, which produces acidic ketone bodies. [3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH and keto acids in either the blood or urine. [1] The primary treatment of DKA is with intravenous fluids and insulin. [1]