Ammoniogenesis

Ammoniogenesis is the process of formation of ammonia (NH3) in the body. Ammonia is a toxic substance, so the body tries to keep its levels low. However, in some cases, increased ammonia formation may occur, leading to the development of hyperammonemia and ammonium acidosis.

Ammonia is formed in the liver during protein metabolism, mainly during the deamination of amino acids. Another source of ammonia is the breakdown of urea by intestinal microflora. Normally, ammonia is mainly utilized in the liver in the urea cycle and is partially excreted by the kidneys in the urine.

Increased ammoniogenesis can be caused by hereditary diseases of amino acid metabolism and the urea cycle, liver diseases accompanied by a violation of its detoxification function, as well as excessive bacterial breakdown of urea in the intestine. Effective treatment of hyperammonemia is aimed at eliminating its causes.

Ammoniogenesis is the process of formation of ammonia in the human stomach or intestines. It comes from amino acid compounds such as the amino acids glutamic acid and glycine, which can be obtained from food or produced in the intestines. This process is an important step for many organisms as it allows them to obtain energy using ammonia as a source of nitrogen.

However, this process may not be desirable for humans, as excess ammonia can lead to increased levels of acidity in the stomach and lead to diseases such as acid reflux and stomach ulcers.

Ammoniogenesis begins in the cells of the gastric mucosa and ends in the terminal intestine. Glutamine, one of the amino acids found in food, and two other amino acids - glycine and cysteine ​​- are synthesized by bacteria found in the intestines using the enzyme glutamine synthetase.

Glutaminase, which converts glutamate back to glutamine in the presence of ammonia, and glutamic aminotransferase, which uses glutamine to form amino acids like glycine, are the main enzymes involved in converting glutamate acids into the body's essential amino acid, glutamine. This occurs through the process of cyclization (periodically increasing the level of glutamate).

Once glutamine is converted back to cystenine and glycine, they must enter the epithelial cells of the intestinal mucosa for further use by the body. This involves the reversal of glutamine-resistant amidine transporters in enterocytes to allow the passage of these compounds from the intestinal lumen into the intestinal wall through the membrane. They then penetrate the epithelial tissues of the crypt/crypt and provide the levels of amino acids (glutamate, cismethamindine and glycine) necessary to restore glutamine stores in the nutritional systems within the cells. Glutamate is then processed in the intestinal mucosa by glutamate oxidase to produce glutamine dioxide and regenerate ammonia. Remains of glutamine dioxide that are not present in the bloodstream are reversely metabolized during ammoniosis, and are then excreted from the body, being transported back through the synthetic phase by cystites into the bloodstream. Cystamine bound to cystic acids is captured by tamps, liver enzymes to aid regeneration into glutamic acids, which then enter into reserve compounds until the supply of glutamin is renewed. After several hours of exchange, glutamatic acid can be reabsorbed through enteral endocytosis. This interconnected cycling of glutamate dioxide synthesis is an important part of amino acid metabolism and ensures constant