Does proteolysis explain glutamine release from the septic brain.docVIP

Dejong and Olde Damink Critical Care 2010,14:152 /content/14/3/152 COMMENTARY Does proteolysis explain glutamine release from the septic brain? Cornelius HC Dejong* and Steven WM Olde Damink See related research by Berg et al., /content/14/1/R16 data are interesting and important, but there are some Abstract issues that should be highlighted to put the data in Berg and colleagues report on amino acid exchange context. ese issues relate to the analogy with the across the human brain during endotoxin infusion. Lipopolysaccharide infusion induced a decrease in the ratio between branched chain amino acids and aromatic amino acids, increased unidirectional phenylalanine uptake, and increased net brain glutamine release. Cerebral proteolysis is suggested to play a role, but the question is whether this is the case and why this would happen. situation in hepatic encephalo pathy, the accuracy of ? ux measurements, and the potential role of cerebral protein breakdown. During liver failure and associated hyperammonemia, ammonia is detoxi? ed mainly in the brain and muscle by the formation of glutamine from ammonia and gluta- mate. In muscle, BCAA transaminate with α-ketogluta- rate, yielding glutamate – which may lower plasma BCAA. Ammonia may then be coupled to glutamate to form glut is glutamine can subsequently be Berg and colleagues report on the net exchange of amino acids and ammonia across the brain in healthy volunteers before and 1 hour after a 4-hour endotoxin infusion [1]. Amino acids and ammonia were measured in arterial and exported from the brain (and muscle), which in essence means loss of glutamate, an important excitatory neurotransmitter. e increased cerebral release of glutamine during hyper ammon emia could facilitate venous plasma, and cerebral blood ? ow was measured. exchange of glutamine for neutral amino acids, notably Lipo