GLUTAMINE AND GLUCOSE HOMEOSTASIS

In critically ill patients, glycemic control is an important issue (Falciglia et al. 2009; Preiser et al. 2002) and the use of intensive insulin therapy with tight glycemic control has been extensively debated in the past few years (Marik and Preiser 2010; Treggiari et al. 2008; van den Berghe et al. 2001). In the French multicenter, randomized, controlled study evaluating the effects of intravenous glutamine, reduced hyperglycemia episodes and insulin needs have been observed in critically ill patients (Dechelotte et al. 2006). This reduction of insulin resistance by glutamine has been confirmed by others (Grau et al. 2011; Grintescu et al. 2015). Studies in healthy controls indicate that enteral infusion of glutamine increased the insulin level (Bouteloup et al. 2000; Coeffier et al. 2003). Recent data indicated that glutamine may affect incretin production (Joshi et al. 2013). Supplementation with glutamine of obese mice resulted in persistent reductions in both plasma glucose and insulin levels (Opara et al. 1996). In dogs, glutamine infusion markedly increased whole-body glucose utilization, mainly muscular and hepatic, and also increased whole-body glucose production to some extent (Borel et al. 1998). In addition, parenteral Ala-Gln administration attenuated insulin resistance and improved glucose utilization in multiple-trauma patients (Bakalar et al. 2006). Thus, glutamine may have potential benefits during clinical situations associated with insulin resistance.