Nutrients can impact and regulate cellular metabolism and cell function which is particularly important for the activation and function of diverse immune subsets. Among the critical nutrients for immune cell function and fate, glutamine is possibly the most widely recognised immunonutrient, playing key roles in TCA cycle, heat shock protein responses and antioxidant systems. In addition, glutamine is also involved with inter-organ ammonia transport, and this is particularly important for not only immune cells, but also to the brain, especially in catabolic situations such as critical care and extenuating exercise. The well characterised fall in blood glutamine availability has been the main reason for studies to investigate the possible effects of glutamine replacement via supplementation but many of the results are in poor agreement. At the same time, a range of complex pathways involved in glutamine metabolism have been revealed via supplementation studies. This article will briefly review the function of glutamine in the immune system, with emphasis on metabolic mechanisms, and the emerging role of glutamine in the brain glutamate/gamma-amino butyric acid cycle. In addition, relevant aspects of glutamine supplementation are discussed.

In chickens, metabolism is influenced by environmental factors and of particular interest nutritional factors, such as diet quantity and composition. With respect to the dietary macronutrients, literature clearly shows that in isoenergetically formulated diets, the protein level has a pronounced effect on metabolism, whereas fat and carbohydrate concentrations play a limited role. A decreased dietary protein level results in depressed growth rates, with reduced carcass gains in both water and protein content. In spite of the lower protein retention in chickens fed low protein diets, the efficiency of utilization of dietary protein appears to be increased. This indicates an inverse relationship between protein intake and utilization, which is reflected in decreased circulating uric acid levels. In addition, feed intake is increased, at least when protein levels are slightly reduced, leading to an involuntary overconsumption of energy compared to protein. The chickens deal with this excess energy consumption by increasing de novo lipogenesis and fat deposition, which is supported by increased plasma triglyceride concentrations, and heat production is increased. In contrast to adult mammals, the dietary macronutrients have no effect on diet-induced thermogenesis, nor is there any relationship between diet-induced thermogenesis and feed intake. Plasma growth hormone levels are higher in chickens reared on a low protein diet, indicating a causal relationship between growth hormone secretion and protein efficiency. In spite of the increased growth hormone levels, plasma insulin-like growth factor concentrations are lowered in low protein reared chickens, and may be partially responsible for the reduced growth rate observed in these animals. Plasma corticosterone concentrations are augmented in chickens on low protein diets, despite a decline in the ACTH concentration. Finally, plasma T3 and T4 levels are well known to increase and decrease, respectively, with decreasing protein content, whereas the effects of dietary macronutrients on circulating leptin levels require more research.