Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malnutrition is a common complicating factor in surgical illness. To investigate the cellular changes and mechanisms responsible for the protein wasting associated with nutritional deprivation, Sprague-Dawley rats were subjected to total protein-calorie starvation for 3 (n = 12) or 5 days (n = 12) and compared to freely fed animals monitored for 3 (n = 8) or 5 (n = 8) days. Gastrocnemius protein and RNA content and levels of mRNA coding for the myofibrillar proteins myosin heavy chain, myosin light chain, and alpha-actin were measured. Starvation resulted in a significant decrease in gastrocnemius mass and protein content, and was associated with decreases in mRNA levels for the three myofibrillar proteins assayed. We conclude that changes in mRNA levels for these proteins likely contribute to the loss of peripheral protein which occurs during total nutritional deprivation. In addition, the changes in mRNA levels for these three structural proteins appear to be coordinate, suggesting that transcription of no single myofibrillar protein is rate-limiting in the regulation of skeletal muscle protein content.
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PMID:Starvation leads to decreased levels of mRNA for myofibrillar proteins. 249 68

Macrophage secretory products are suspected to participate in the severe lean tissue wasting related to chronic illness. The protein metabolic effects of chronic, 7-day cachectin/tumor necrosis factor (cachectin) or interleukin 1 alpha (IL-1 alpha) administration in vivo were studied in male Wistar rats that were 1) freely fed, 2) pair fed, 3) total protein and calorie starved, 4) twice daily lipopolysaccharide (LPS) administered, 5) twice daily cachectin administered, and 6) twice daily IL-1 alpha administered. LPS, cachectin, or IL-1 alpha administration produced anorexia; weight loss in these groups was comparable to respective pair-fed animals. However, LPS, cachectin, or IL-1 alpha accelerated peripheral protein wasting while preserving liver protein content, unlike the pattern in the pair-fed or starved animals in which loss of liver proteins and relative preservation of skeletal muscle protein were observed. The decrease in skeletal muscle protein content in LPS- or cytokine-treated animals was associated with coordinate decreases in muscle mRNA levels for the myofibrillar proteins myosin heavy chain, myosin light chain, actin, and in the 18S and 28S subunits of ribosomal RNA. We conclude that chronic exposure to the cytokines, IL-1 alpha or cachectin, can simulate those body and muscle protein changes seen in experimental LPS administration or chronic disease and markedly differ from the pattern of protein redistribution due to caloric restriction.
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PMID:Cachectin/TNF or IL-1 alpha induces cachexia with redistribution of body proteins. 278 90

A patient with polymyositis manifesting severe myocardial damage and conduction block is described. A 57-year-old man presented dysarthria, dysphagia, proximal-dominant muscle weakness and wasting of the extremities. Muscle biopsy revealed degeneration and regeneration of muscle fibers and infiltration of mononuclear cells. After admission, muscle weakness rapidly progressed and mechanical ventilation was needed for respiratory failure. Simultaneously, cardiac symptom developed and resulted in bradycardia and trifascicular conduction block, which required a pacemaker. Echocardiogram revealed diffuse hypokinesia, ventricular enlargement and thickened wall. Marked elevations of serum CK-MB, cardiac myosin light chain I and cardiac troponin T were observed. High dose administration of methylprednisolone resulted in improvement of muscular and cardiac symptoms, and prevented complete heart block. Immediate and high dose of steroid therapy was considered to be effective for severe myocarditis in polymyositis.
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PMID:[A patient of polymyositis with severe myocardial damage and conduction block]. 1039 Oct 81