Glutamine deficiency as a cause of human immunodeficiency virus wasting

Nutritional Treatment for Acquired Immunodeficiency Virus‐Associated Wasting Using β‐Hydroxy β‐Methylbutyrate, Glutamine, and Arginine: A Randomized, Double‐Blind, Placebo‐Controlled Study

“…Glutamine muscle glutamine appears to be a major regulator of < muscle proteolysis. 17,25,26 Arginine is the precursor to nitric oxide in the body27 which is thought to play a role in nitrogen sparing effect in trauma '28 wound healing,l7°29 and immune stimulation.27,3o Last, HMB is thought to exert a protective effect on muscle such that processes causing muscle damage and muscle proteolysis are minimized.2o,31 HMB supplementation has been shown to markedly decrease the exercise-induced damage in muscle. The mechanism by which HMB slows muscle protein breakdown is not fully understood 21 but it is likely that HMB is acting on muscle by mechanism(s) distinct from those of arginine and glutamine.…”

Protective Effect of Glutamine from Glucocorticoid-Induced Muscle Atrophy Occurs without Alterations in Circulating Insulin-Like Growth Factor (IGF)-I and IGF-Binding Protein Levels

“…Along these same lines, potential glutamine depletion exists in athletes experiencing the overtraining syndrome as well as in individuals engaged in intense interval training, where depressed blood glutamine levels have been reported (24)(25)(26)(27). Most recently, it has been proposed that glutamine deficiency may explain the progression of muscle wasting that is found during human immunodeficiency virus infection (28). Moreover, initial support for glutamine's positive impact comes from clinical investigations.…”

The Cytokine Basis of Cachexia and its Treatment: Are They Ready for Prime Time?

“…213,214 It is hypothesized that enhanced production of acute-phase proteins in the liver during a hypercatabolic process like cachexia depletes the available pool of critical amino acids like glutamine, thereby decreasing the synthesis of myofibrillar muscle proteins. [215][216][217][218] TNF-␣, IL-6, and IL-1 are principal pro-inflammatory cytokines inducing the acute phase response of the liver. 219,220 Pouliquen reviewed the literature of glioma-induced cachexia in rats and postulated that the decrease in relative liver mass and the increase in resting energy expenditure could be accounted for by the increased activity of the Cori cycle, which caused increased shunting of the intermediary metabolic steps in the liver toward energy use rather than energy storage.…”