METABOLIC STATES ASSOCIATED WITH POSITIVE EFFECTS OF GLUTAMINE SUPPLEMENTATION

In certain states associated with insulin resistance, an apparent increased tissue requirement for glutamine occurs, often resulting in low levels of plasma glutamine (Borel et al. 1998). These include Type 2 Diabetes Mellitus (T2DM) (Samocha-Bonet et al. 2011), severe exercise (Iwashita et al. 2005), and catabolic settings such as seen in burns (Peng et al. 2006), trauma (Bakalar et al. 2006; Dechelotte et al. 2006), surgery (Wilmore 2001; Dechelotte et al. 2006; Awad and Lobo 2012; Cui et al. 2014), sepsis and fasting, including perioperative fasting (Awad and Lobo 2012). A normal dietary intake of <10 g plus the endogenous production of 40-70 g per 24 h (Tjader et al. 2007) would thus appear to be insufficient for the increased demand in spite of increased release of glutamine from skeletal muscle and accelerated synthesis (Lacey and Wilmore 1990) under these conditions. A summary of metabolic changes associated with the catabolic state can be found in Figure 4.1. Biological requirements for glutamine clearly differ between homeostatic and catabolic bioenergetic states. Thus it is possible that glutamine supplementation may have different effects on insulin action and glycemic control in these different states.

To counteract glutamine depletion in catabolic states, supplementation studies have been undertaken in varying contexts. While two clinical studies found glutamine supplementation may have a negative effect on glycemic control (Duska et al. 2008; Breitman et al. 2011), many others found patient outcomes (e.g., rate of infection, length of time on ventilator or in ICU, and nitrogen balance) improved with glutamine intake (Iwashita et al. 2005; Dechelotte et al. 2006; Bakalar et al. 2006; Grau et al. 2011; Hissa et al. 2011; Samocha-Bonet et al. 2011; Dock-Nascimento et al. 2012; Bashandy et al. 2013). This was often ascribed to its effect on insulin action, where observed improvements in glycemic control (Dechelotte et al. 2006; Grau et al. 2011; Hissa et al. 2011; Samocha-Bonet et al. 2011) were attributed to an attenuation of insulin resistance (Bakalar et al. 2006; Bashandy et al. 2013; Cui et al. 2014). A summary of these studies follows, including studies on healthy subjects and trauma patients, diabetics and animal models. It is important to note that variations in several factors may influence results and the interpretation of the effect of glutamine on insulin action. These include (a) differences in delivery, including oral, parenteral, and enteral delivery; (b) differences in administration, including glutamine given in isolation, in an amino-acid cocktail, in combination with either free alanine or as the alanyl-glutamine dipeptide, or with lipids or other substances such as growth hormone; and (c) differing metabolic states of recipients, ranging from healthy, through T2DM to severely catabolic such as in major trauma. These variations can, for example, affect activation of gut hormones, confound or compliment results, or otherwise affect physiologic response (Table 4.1).

 
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