Barbosa Rômulo Cesar Costa, Guimarães Sergio Botelho, de Vasconcelos Paulo Roberto Cavalcante, Chaves Carolyne Rolim, de Vasconcelos Paulo Roberto Leitão
Department of Surgery, UFC, Fortaleza, CE, Brazil.
Burns. 2006 Sep;32(6):721-7. doi: 10.1016/j.burns.2005.12.014. Epub 2006 Aug 4.
Burn injury elicits a sustained hypermetabolic state characterized by accelerated hepatic synthesis of amino acids and proteolysis leading to negative nitrogen balance. This paper was aimed at studying the effects l-alanyl-glutamine (Ala-Gln) exogenous offer to rats submitted to thermal burn. Twenty-four anesthetized male Wistar rats were submitted to scald burn of dorsal skin (30% body surface). Eighteen and 42-h later rats were randomized to receive (by gavage) 2ml of water (G-1) or equal volume (0.5g/kg weight/day) of Ala-Gln solution (G-2). Tissue and blood samples were collected at the end of 24 and 48-h post-burn trauma (PBT). Blood concentrations of metabolites (glucose, pyruvate, lactate and ketone bodies) were similar in all groups. There were significant differences in tissue metabolites concentrations in Ala-Gln treated rats (G-2) compared to control (G-1) following scald injury. The administration of Ala-Gln to burned rats induces a fall ATP (muscle, healthy skin), pyruvate and ketone bodies (liver) concentrations 24-h PBT. It also induces significant increase of lactate (burned skin) 24-h and glucose (liver) 28/48-h PBT. Rise of tissue lactate concentrations may be due to enhanced anaerobic glycolysis resulting from increased availability of glutamate, derived from glutamine, with possible activation of the malate-aspartate shuttle.