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Ketone bodies

Synonym: keto body
English: ketone bodies

1 definition

To the so-called Ketone bodies include the chemical compounds acetoacetate, acetone and beta-hydroxybutyrate. The latter is counted among the ketone bodies, although chemically it is a hydroxycarboxylic acid.

2 physiology

When there is an absolute or relative lack of carbohydrates, ketone bodies are created as a by-product of fat burning in the mitochondria of the liver cells (hepatocytes) - for example, when people are hungry. The formation of ketone bodies is essential for the brain's metabolism, as they are the only source of energy alongside glucose.

Another reason is a reduced absorption of glucose in the context of diabetes mellitus. The glucose level in the blood is not necessarily reduced. If there is a lack of insulin, the glucose concentration is high, but the carbohydrate cannot be absorbed by the cells and used ("relative glucose deficiency").

As part of a ketogenic diet, the formation of ketone bodies is specifically induced by a low-carbohydrate diet.

3 synthesis (ketogenesis)

The synthesis of ketone bodies is known as ketogenesis. If there is a lack of carbohydrates, more fatty acids are broken down via beta-oxidation to acetyl-CoA. At the same time, there is a lack of oxaloacetate, to which acetyl-CoA is normally bound in the citric acid cycle. As a result, acetyl-CoA accumulates in the hepatocytes. This serves as a substrate for the synthesis of ketone bodies, which takes place in the matrix space of mitochondria.

3.1 Regulation of the synthesis

The synthesis is regulated by three enzymes.

3.1.1 Hormone-sensitive lipase

The phosphorylated hormone-sensitive lipase (HSL) hydrolyzes triacylglycerols to fatty acids and these are then broken down in the beta-oxidation process. This leads to an increased concentration of acetyl-CoA. The HSL is largely regulated by adrenaline and insulin. Adrenaline activates the HSL as part of lipolysis. Insulin causes dephosphorylation and thus inactivation of the enzyme.

3.1.2 Acetyl-CoA carboxylase

Acetyl-CoA carboxylase converts acetyl-CoA into malonyl-CoA. This causes less acyl-CoA, the substrate of beta-oxidation, to be transported into the mitochondria. Insulin stimulates this enzyme.

3.1.3 HMG-CoA synthase

Insulin inhibits the enzyme while it is activated by food abstinence and very high-fat foods.

4 Breakdown of ketone bodies

The liver releases ketone bodies into the blood because it cannot metabolize them. They serve numerous extrahepatic tissues (especially the CNS) as a source of energy. In order to be introduced into the oxidative metabolism, however, they must first be activated:

  • At the beginning, beta-hydroxybutyrate is oxidized to acetoacetate.
  • This is followed by the reaction of acetoacetate with succinyl-CoA, whereby acetoacetyl-CoA and succinate are formed.
  • After the acetoacetyl-CoA has been cleaved to acetyl-CoA by the 3-ketothiolase, it can be introduced into the citric acid cycle as acetyl-CoA.

5 diabetic ketoacidosis

Diabetic ketoacidosis occurs primarily in patients with type 1 diabetes mellitus and results from a pronounced insulin deficiency and increased concentrations of glucagon, cortisol and catecholamines.

This causes, among other things, an activation of the hormone-sensitive lipase and thus a hydrolysis of triacylglycerols, which in turn increases the concentration of free fatty acids. This ultimately leads to an increased concentration of acetyl-CoA, from which more ketone bodies are synthesized. The pH of the blood falls (metabolic acidosis) as acetoacetate and beta-hydroxybutyrate dissociate. Acetone, on the other hand, is exhaled through the lungs.

6 detection methods

Higher levels of ketone bodies are noticeable by the characteristic acetone odor of the exhaled breath. In laboratory tests, ketone bodies can be detected semiquantitatively in blood and urine (ketonuria) using test strips (Legal's test, nitroprusside method). These only react with acetoacetate and acetone, but not with beta-hydroxybutyrate.