摘要:

Purpose of reviewWasting of muscle mass, commonly present in patients with chronic obstructive pulmonary disease, is a complex process involving changes in the control of intermediary metabolism as well as in muscle cell status. Although research exploring intermediary metabolism in chronic obstructive pulmonary disease is still in its infancy, there is an increased interest in a potential role for amino acids in modulating muscle anabolism. This review aims at summarizing and critically evaluating the available clinical studies examining alterations in amino acid profile in plasma and skeletal muscle of patients with chronic obstructive pulmonary disease.Recent findingsAll studies show pronounced alterations in plasma and muscle amino acid status in patients with chronic obstructive pulmonary disease but no consistent ‘disease specific’ pattern for most amino acids. Variability is likely influenced by the heterogeneity of the disease with respect to lung function and nutritional state. Nevertheless, general consistency exists in chronic obstructive pulmonary disease with respect to (1) a reduced plasma branched-chain amino acid level, and (2) a decreased muscle glutamate concentration. Alterations in branched-chain amino acid metabolism appear to be influenced by the degree of muscle wasting, while the reduction in muscle glutamate is related to the diffusing capacity as a hallmark of emphysema. The reduction in glutamate status is associated with reduced muscle glutathione levels and appears to be linked to enhanced glycolysis as evidenced from an accelerated increase in plasma lactate during exercise.SummaryUnderlying mechanisms of the observed alterations in amino acid profile in chronic obstructive pulmonary disease, and the influences of disease associated mediators such as chronic low-grade inflammation and (chronic and intermittent) hypoxia are speculative and need to be explored in experimental study designs.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewLiver cirrhosis in the advanced state is characterized by protein wasting, as indicated by the loss of muscle mass, hypoalbuminemia, and an abnormal amino acid profile. The protein wasting condition cirrhosis is associated with a poor prognosis and reduced survival. Poor nutrition, metabolic and hormonal abnormalities, and other disease-associated alterations may all concur to protein wasting. An understanding of the causes and mechanisms leading to protein wasting in cirrhosis may help in the development of nutritional interventions and new therapies.Recent findingsAlbumin and muscle protein turnover in cirrhotic patients have been studiedin vivowith the aid of isotope dilution techniques or organ catheterization. Albumin synthesis appears to parallel liver function, i.e. the more compromised is the liver, the less is the albumin production rate. Meal-induced albumin synthesis is impaired even in compensated cirrhotic patients. Skeletal muscle protein synthesis is diminished in cirrhosis, and total muscle protein breakdown also appears to be increased, thus explaining the reduced muscle mass. Either hormone or substrate resistance, or newly involved substances (cytokines, insulin-like growth factor 1, leptin) may play a role in the reduced synthesis of both albumin and muscle proteins in liver cirrhosis.SummaryAbnormalities of both albumin and muscle protein turnover have been demonstrated in liver cirrhotic patients. The possible role of the multiple hormonal and metabolic abnormalities of this disease, as well that of cytokines and other recently discovered substances, need to be investigated further.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewThe objective is to summarize the findings from recent (June 2001-2002) studies that have examined the potential benefits of exercise training for the treatment of wasting associated with sarcopenia, cancer, chronic renal insufficiency, rheumatoid arthritis, osteoarthritis and HIV. In many clinical conditions, protein wasting and unintentional weight loss are predictors of morbidity and mortality. The pathogenesis of protein wasting in these conditions can be different, but the fundamental mechanism is an imbalance between muscle protein synthetic and proteolytic processes. The muscle proteins most affected and the precise alterations in their synthetic and proteolytic rates that occur in each cachectic condition are still under investigation.Recent findingsRegular exercise, or sometimes just a modest increase in physical activity, can mitigate muscle protein wasting. Aerobic exercise training primarily alters mitochondrial and cytosolic proteins (enzyme activities), while progressive resistance exercise training predominantly increases contractile protein mass. Previous studies indicate that resistance exercise acutely increases the muscle protein synthetic rate more than muscle proteolysis such that the muscle amino acid balance is increased for up to 2 days after exercise. Progressive resistance exercise training increases muscle protein synthesis and muscle mass, but attenuates the increment in proteolysis that results from a single bout of resistance exercise. The cellular mechanisms that produce these adaptations are not entirely clear.SummaryIn general, patients with wasting conditions who can and will comply with a proper exercise program gain muscle protein mass, strength and endurance, and, in some cases, are more capable of performing the activities of daily living.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewIn response to decreased usage, skeletal muscle undergoes adaptive reductive remodeling due to the decrease in tension on the weight bearing components of the musculo-skeletal system. This response occurs with uncomplicated disuse (e.g. bed rest, space flight), as a secondary consequence of several widely prevalent chronic diseases for which activity is reduced (e.g. chronic obstructive pulmonary disease and chronic heart failure) and is part of the aging process. The problem is therefore one of considerable clinical importance.Recent findingsThe impaired function and exercise intolerance is related more to the associated muscle wasting rather than to the specific organ system primarily impacted by the disease. Progress has continued in describing the use of anabolic drugs and dietary manipulation. The major advance in the field has been: (i) the discovery of the atrogin-1 gene and (ii) the application of microarray expression analysis and proteomics with the objectives of obtaining comprehensive understanding of the pathways changed with disuse atrophy.SummaryDisuse atrophy is a common clinical problem. There is a need for therapeutic interventions that do not involve exercise. A better understanding of the changes, particularly at the molecular level, could indicate hitherto unsuspected sites for nutritional and pharmacological intervention.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Purpose of reviewNitric oxide is an important mediator of both physiological and pathophysiological processes. Nitric oxide is produced during direct conversion of arginine to citrulline. Nitric oxide is rapidly metabolized, mainly to nitrite/nitrate, and finally excreted as urinary nitrate. For that reason, plasma and urinary nitrite/nitrate have been measured frequently as indicators of nitric oxide production, but it is becoming clear that these methods only give qualitative data. More recently, stable isotope methods have been introduced for quantitative measurement of nitric oxide production. This review aims at summarizing and evaluating these isotopic investigations of nitric oxide metabolism in disease.Recent findingsDifferent stable isotope methods are used to measure whole body nitric oxide productionin vivo. These methods are all based on infusion of guanidino-labeled L-arginine and subsequent measurement of labeled products (e.g. nitrite/nitrate or citrulline). Nitric oxide synthesis in healthy individuals is found to be in the range of 0.2-1.0 μmol kg−1h−1, only 0.5-1% of arginine production. In diseased states, nitric oxide synthesis was found to be either decreased or increased. Increased nitric oxide synthesis was observed in gastroenteritis patients and in some animal models of sepsis. In patients with renal failure, however, both increased and decreased nitric oxide production have been reported. Nitric oxide production was not changed in familial hypercholesterolemia patients and after typhoid vaccination.SummaryUsing stable isotopes to measure whole body nitric oxide productionin vivois the most accurate method to study quantitative changes in the nitric oxide production rate. This technique is easy to perform in both healthy and diseased individuals, requiring infusion of stable isotopes for only a few hours and blood sampling.

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:1363-1950    

出版商:OVID    

年代:2003

数据来源: OVID