This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.In diabetes, the lack of insulin leads to incomplete suppression of gluconeogenesis despite an elevated blood glucose level and increased mobilization of free fatty acids (FFA), amino acids and other organic acids into the circulation. This chronic increased acid load necessitates renal compensation with increased urinary NH4+ excretion. When there is an inability to compensate completely, a metabolic acidosis develops, and when severe, is known as diabetic ketoacidosis. The excess acid can be harmful and correcting the acidosis is the goal of treatment of DKA. In diabetic rat studies, Lemieux et al. found that administration of glutamine increases the amount of ammonium (acid) in the urine and the amount of sugar in the body makes when the rats have DKA. If intravenous glutamine increases the amount of ammonium (acid) in the urine of children with DKA, this may help to reduce the amount of acid in the blood. The purpose of this study is to investigate the effect of giving intravenous glutamine in the form of 'glycyl-L-glutamine' to children with DKA and to determine if this treatment will help correct the acidosis faster. We will also determine if these children require less supplementation of sugar during their therapy.
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