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l-glutamine has many important biological functions within the human body. It is an important fuel for the intestinal mucosal cells, hepatocytes and rapidly proliferating cells of the immune system, assists in the regulation of acid balance thus preventing acidosis, acts as a nitrogen shuttle protecting the body from high levels of ammonia, and is involved in the synthesis of amino acids (including l-glutamate), GABA, glutathione (an important antioxidant), purine and pyramidine © 2007 Elsevier Australia

nucleotides, amino acid sugars in glycoproteins and glycans, and nicotinamide adenine dinucleotide (NAD). It is also involved in protein synthesis and energy production (Boelens et al 2001, Kohlmeier 2003, Miller 1999, Niihara et al 2005, Patel et al 2001, PDRHealth 2006a). GASTROINTESTINAL PROTECTION/REPAIR

According to in vitro and in vivo research, L-GIn aids in the proliferation and repair of intestinal cells (Chun et al 1997, Rhoads et al 1997, Scheppach et al 1996) and is the preferred respiratory fuel for enterocytes (and also utilised by colonocytes) (Miller 1999). It is thus vital for maintaining the integrity of the intestinal lining and preventing the translocation of microbes and endotoxins into the body. In addition, L-Gln helps to maintain secretory IgA, which functions primarily by preventing the attachment of bacteria to mucosal cells (PDRHealth 2006a, Yu et al 1996).

According to evidence from animal studies it may also assist in preventing atrophy following colostomy (Paulo 2002) and irradiation (Diestel et al 2005), and intestinal injury by inhibiting intestinal cytokine release (Akisu et al 2003). L-glutamine depletion induces apoptosis by triggering intercellular events that lead to cell death (Paquette et al 2005), resulting in altered epithelial barrier competence (increased intestinal permeability), bacterial translocation, and increased mortality. Under experimental conditions, L-GIn may assist in maintaining intestinal barrier function by increasing epithelial resistance to apoptotic injury, reducing oxidative damage, attenuating programmed cell death and promoting re-epithelialisation (Masuko 2002, Ropeleski et al 2005, Scheppach et al 1996) and may thus reduce bacterial and endotoxin translocation (Chun etal 1997).

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