摘要:

Purpose of reviewThe aim of this review is to describe the clinical relevance of supplementation of glutamine from the recent literature. First, new basic research is examined and subsequently recent clinical trials and a metaanalysis are illustrated.Recent findingsGlutamine has a major impact on the functionality of the immune system. It has recently been established that glutamine not only has a protective effect on cells of the immune system, but also on other cells of the body, for instance cardiomyocytes. Evidence is accumulating for an effect of glutamine via glutathione, heat shock proteins as well as taurine. Another area of interest is the way glutamine enhances gut barrier function. More and more research is concentrating on the positive effect of glutamine on the gut-associated lymphoid tissue.SummaryBased on a recent meta-analysis and up-to-date clinical trials, we may conclude that glutamine has a beneficial effect on infectious complications and reduces hospital stay. In critically ill patients glutamine supplementation may reduce morbidity and mortality. The greatest effect was observed in patients receiving high dose parenteral glutamine. A recent study with high dose enteral glutamine demonstrated a reduced mortality in the glutamine supplemented group. In the future more trials with larger numbers of participants are needed, especially with high dose enteral glutamine in the perioperatively and the intensive care unit setting.

ISSN:1363-1950    

出版商:OVID    

年代:2004

数据来源: OVID

摘要:

Purpose of reviewThe application of tracer kinetic methods, combined with measurements of the activity of components of the cellular signaling pathways involved in protein synthesis and degradation, affords new insights into the regulation of skeletal muscle protein metabolismin vivoin humans. Feeding is associated with an increase in protein synthesis and a decrease in proteolysis. These changes are mediated by feeding-induced increases in plasma concentrations of both nutrients and hormones.Recent findingsRecent studies definitely demonstrated that insulin and amino acids directly interacted in promoting postprandial anabolism. However, the contribution of amino acids was abolished in old individuals in whom only insulin action persisted. There was a line of evidence that the effect of amino acids originates from leucine, which should not be viewed simply as a building block for protein synthesis, but as a signal in the regulation of cell functions. Although their cellular signaling pathways do not completely overlap, insulin and amino acids both activate the translation initiation of protein synthesis. Insulin presumably inhibits skeletal muscle protein degradation through a decrease in the activity of the ubiquitin proteasome-dependent pathway.SummaryWhether or not amino acids modify insulin action and have specific effects on proteolysis has not yet been documented. At the molecular level, amino acids such as insulin modulate gene expression. Such studies are needed to gain a better understanding of the interactions between insulin and amino acids in the regulation of skeletal muscle protein anabolism.

ISSN:1363-1950    

出版商:OVID    

年代:2004

数据来源: OVID

摘要:

Purpose of reviewThis review reports recent findings on the effect of enterally fed protein and amino acids on metabolism, function, and clinical outcome, particularly during the neonatal period.Recent findingsSplanchnic tissues metabolize significant proportions of some enteral amino acids and this likely contributes to the higher requirement for these amino acids when they are provided enterally versus parenterally. Splanchnic tissues are particularly key in the provision of nutrition to preterm infants, who possess an exceedingly high protein anabolic drive, but limited tolerance to aggressive enteral feeding. The protein anabolic response to specific proteins is influenced by the rate of digestion and the pattern of feeding, as well as the amino acid composition of the proteins. The post-prandial rise in amino acids and insulin stimulates neonatal tissue protein synthesis by modulation of the nutrient and insulin signaling pathways that lead to translation initiation. A flurry of investigations into the metabolic response and clinical impact of individual amino acids suggests that leucine, glutamine, and arginine, in particular, have specific roles in regulating protein synthesis and immune function.SummaryRecent findings suggest that enteral nutrition support that provides an optimum combination of proteins and amino acids can have a beneficial impact on the clinical outcome of patients.

ISSN:1363-1950    

出版商:OVID    

年代:2004

数据来源: OVID

摘要:

Purpose of reviewNutritional status is an important predictor of clinical outcome in chronic hemodialysis patients, as uremic malnutrition is strongly associated with an increased risk of death and hospitalization events. Decreased muscle mass is the most significant predictor of morbidity and mortality in these patients. Several factors that influence protein metabolism predispose chronic hemodialysis patients to increased catabolism and the loss of lean body mass. The purpose of this review is to discuss recent advances in the understanding of abnormalities in protein homeostasis in chronic hemodialysis patients.Recent findingsIt has long been suspected that the hemodialysis procedure is a net catabolic event. Recent studies have indeed shown that the hemodialysis procedure induces a net protein catabolic state at the whole-body level as well as in skeletal muscle. There is evidence to suggest that these undesirable effects are caused by decreased protein synthesis and increased proteolysis. The provision of nutrients, either in the form of intradialytic parenteral nutrition or oral feeding during hemodialysis, can adequately compensate the catabolic effects of the hemodialysis procedure. Whereas the mechanisms of these effects have not been studied in detail, changes in extracellular amino acid concentrations and certain anabolic hormones such as insulin are important mediators of these actions.SummaryThere is now indisputable evidence to suggest that the hemodialysis procedure leads to a highly catabolic state. Despite this, chronic hemodialysis patients can still achieve anabolism when given adequate protein supplementation to meet the metabolic requirements of hemodialysis, and when adequate insulin is present.

ISSN:1363-1950    

出版商:OVID    

年代:2004

数据来源: OVID

摘要:

Purpose of reviewMitochondria are the site of oxidative substrate utilization to produce adenosine triphosphate for normal tissue function. Tissue substrate utilization is impaired in ageing and type 2 diabetes. Defects in mitochondrial gene expression, protein synthesis and function occur with ageing in various tissues including skeletal muscle, and are emerging in individuals with type 2 diabetes. The current review will discuss advances in the understanding of skeletal muscle mitochondrial alterations associated with age and type 2 diabetes.Recent findingsInsulin acutely stimulates skeletal muscle mitochondrial protein synthesis and adenosine triphosphate production. These insulin effects are impaired in insulin-resistant patients with type 2 diabetes who also exhibit defective basal muscle mitochondrial function. The age-related reduction in mitochondrial adenosine triphosphate production has been confirmedin vivoin skeletal muscle in humans and rodents.SummaryThe emerging concept that insulin stimulates mitochondrial protein synthesis and function indicates potential novel molecular mechanisms of metabolic defects in type 2 diabetes, particularly in the post-prandial period characterized by acute increments of plasma insulin concentrations. The potential relationship between insulin resistance and basal post-absorptive muscle mitochondrial defects should be further investigated. As ageing is characterized by insulin resistance, the hypothesis that impaired insulin action could contribute to age-related muscle mitochondrial dysfunction, and metabolic alterations should be addressed.

ISSN:1363-1950    

出版商:OVID    

年代:2004

数据来源: OVID

ISSN:1363-1950    

出版商:OVID    

年代:2004

数据来源: OVID