This paper gives an overview of the metabolism of ammonia, its excretion and detoxification in the human body. Diseases that cause an increase in ammonia concentration are called hyperammonemias. An example of such a disease caused by liver failure is hepatic encephalopathy in which high concentrations of ammonia can cause brain edema due to swelling of astrocytes. A review of animal models that could be used in research of hyperammonemias is given. Best described animal model is the fish model. Fish have six strategies for detoxification of ammonia of which strategies three and six are crucial because they can be compared with the mechanisms of action of ammonia in mammals, related to the synthesis of glutamine and adaptation at the cellular level. In addition to fish other possible animal model are bears in hibernation. They recycle urea without production of ammonia through synthesis of new proteins. Sirtuin is likely involved in the regulation. A new method of treating hyperammonemia is to change host gut microbiome to microbiome which has reduced action of bacterial urease. Bacterial urease can degrade urea in the intestine and thus increase the concentration of ammonia. Further research of mentioned natural animal models is necessary to enable better treatments and reduce mortality due to neurological problems that hyperammonaemias create.