Mediation of burn-induced hypermetabolism by CRF receptor-2 activity

摘要: Hypermetabolism and anorexia are significant problems associated with major burn trauma. Recent studies have implicated hypothalamic peptides receptors of the corticotropin releasing factor (CRF) family as putative mediators burn-induced hypermetabolism. Increased neuronal activity at CRF type 2 receptor (CRF R-2) appeared particularly involved in expression elevated resting energy expenditure (REE) following In present study we continued these investigations R-2 mediation hypermetabolism, demonstrating that 3rd ventricle injection antisense oligodeoxynucleotide (ODN) normalized REE burned rats. Similar treatments or R-1 ODNs had no effect addition, selective antagonist, antisauvagine-30, also reduced significantly rats, while similar treatment antalarmin, was without effect. To determine which endogenous peptide altered measured levels urocortin (UCN) 15 days after injury, finding UCN by nearly 3-fold, level tended to be decreased. We assessed mRNA real-time PCR 7, 14, 21 post-burn, observing decreased 7 UCN-2 alteration UCN-1 any time point. However, each post-burn These results continue suggest increased is integrally one may ligand affecting this receptor.