In sepsis conditions, catabolism of proteins in skeletal muscle is a recurrent feature, but the main regulators are still not identified. Branched‐chain amino acids (AAs) are oxidized to branched‐chain keto acids (BCKAs), which can be used in the TCA cycle. Glutamine (Gln) and alanine (Ala) find their way to kidney and intestine and liver. In the former two, Gln is de‐aminated to glutamate (Glu) and ammonia (NH3), which is removed. Glu and pyruvate can yield Ala and α‐ketoglutaric acid (αKG), which can enter the TCA cycle. Ala is mainly used as a gluconeogenic substrate and is transformed to pyruvate, whereby the NH2 group is removed via the urea cycle. During liver failure, ammonia may leak into the blood, leading to brain damage and coma.