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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparative histochemical and biochemical study of the anterior tibial muscle of 10 alcoholics suggests that neuropathy could be the cause of chronic muscle weakness and wasting. Myopathic changes did not predominate in the findings. It is concluded that the proximal muscle atrophy could also be attributed to neurogenic damage. Histochemical reactions in muscle specimens show a selective type 2 atrophy and a slight increase in the mean diameter of type 1 fibres. Biochemical investigations reveal that the activities of a number of enzymes representative of energy supplying pathways--the glycogenolysis and glycolysis--as well as acid phosphatase activity in the muscle is lowered. Oxidative enzymes are of similar activity in the alcoholics and the control group. The glycolytic enzyme activity is particularly important, being the most sensitive indicators of the onset, intensity, and course of neurogenic damage.
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PMID:Chronic muscle wasting in alcoholics--a histochemical and biochemical study. 209 1

Electromyography, muscle histochemistry and assay of all glycolytic enzymes, phosphorylase, glycogen, carnitine and several mitochondrial marker enzymes in skeletal muscle (vastus lateralis) were carried out in two groups. One group comprised chronic alcoholic patients with prominent proximal wasting, the other was an alcoholic group with normal neuromuscular examination. Biochemical results were compared with data from control groups with normal muscle histology and with non-alcohol related type 2b fibre atrophy. Either 2b atrophy factor or 2b variability coefficient were increased in all wasted alcoholic patients, with normal values in alcoholics without wasting. Electromyography studies were usually normal in proximal muscles, although several patients had mild distal neuropathies. A significant fall in activity of phosphorylase and all glycolytic enzymes was found in wasted alcoholics with reference to normal controls. In the non-ethanolic 2b atrophy group the activity of several glycolytic enzymes was also significantly lower, but for each enzyme the mean activity was not depressed to the same extent as in the wasted alcoholic group. Muscle glycogen, carnitine, and mitochondrial marker enzyme activities (isocitrate dehydrogenase, monoamine oxidase, cytochrome oxidase) were normal in alcoholics with proximal wasting. It is concluded that there is no deficiency of mitochondrial marker enzymes in wasted alcoholics and that a significant depression in glycogenolytic and glycolytic enzyme activity is seen which is explained in part, but probably not fully, by 2b fibre atrophy.
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PMID:Chronic alcoholic proximal wasting: physiological, morphological and biochemical studies in skeletal muscle. 343 19

Eighteen male and 20 female patients who underwent reconstruction of their anterior cruciate ligament (ACL) with a flap from the patellar tendon were randomly assigned into either closed cast, isometric muscle training and electric stimulation (ES group), or closed cast and isometric training alone (control group). The degree of quadriceps wasting was determined from computerized tomographic scans (CT) before and 6 weeks after surgery. Electrical stimulation was given with a battery operated stimulator that produced a rectangular asymmetric balanced biphasic pulse shape. The pulse rate was 40 Hz and the pulse width 300 microseconds. Patients received 30 min of stimulation three times daily during 5.5 weeks. Female control patients showed a larger decrease in quadriceps area on CT than male control patients (P less than .001). No significant difference was found between male electrically stimulated patients and control patients. In female patients, there was on the contrary, a highly significant difference in favor of electrical stimulation (P less than .001) When the different parts of the quadriceps were studied, a significantly lower degree of atrophy of the vastus medialis was found after electrical stimulation. Vastus lateralis did not show any difference. Measurements of CT attenuation, pre- and post-operatively, showed a decrease in attenuation of 17% for the vastus medialis and lateralis of the operated leg after immobilization, indicating an increase in fat content. In the rectus femoris, however, there was an increase in attenuation of 14.6%. Percutaneous muscle biopsies from the vastus lateralis obtained before, one week after, and 6 weeks after surgery revealed that the cross-sectional area of the individual muscle fibers decreased less in the electrically stimulated than in controls, but the difference was not significant. There were no differences between the two groups in the activity of an oxidative enzyme, citrate synthase, or a glycolytic enzyme, phosphofructokinase (PFK). We conclude that females reacted more favorably than males to electrical stimulation of quadriceps during an immobilization period after knee surgery.
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PMID:Prevention of quadriceps wasting after immobilization: an evaluation of the effect of electrical stimulation. 349 82

The comparative electrophysiologic, histochemical, and biochemical investigation of the anterior tibial muscle of 13 alcoholics indicates that neuropathy could be the cause of the chronic muscle weakness and wasting. Myopathic alterations did not predominate in the findings. It was concluded that the proximal muscle atrophy could also be attributed to neurogenic damage. Histochemical reactions in muscle specimens showed a selective type 2 atrophy and a slight increase of the mean diameter of type 1 fibres. Biochemical investigations revealed that the activities of a number of enzymes representative of energy supplying pathways--the glycogenolysis and glycolysis--as well as acid phosphatase activity in the muscle were lowered. A relationship could be assumed between the lowered glycolytic activity and the decline of the mean diameter of type 2 fibres. Oxidative enzymes were of similar activity in the alcoholics and the control group. The glycolytic enzyme activities were particularly important, being the most sensitive indicators of the onset, intensity, and course of neurogenic damage. These activities probably normalise during reinnervation of a muscle earlier than do the morphologic alterations; however, they were markedly lower in alcoholics with impaired liver function and cachexia, probably because of the catabolic metabolic conditions present in these cases.
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PMID:Muscle wasting in chronic alcoholics: comparative histochemical and biochemical studies. 622 Oct 80

Hepatocyte nuclear factors 3 (HNF-3) belong to an evolutionarily conserved family of transcription factors that are critical for diverse biological processes such as development, differentiation, and metabolism. To study the physiological role of HNF-3alpha, we generated mice that lack HNF-3alpha by homologous recombination in embryonic stem cells. Mice homozygous for a null mutation in the HNF-3alpha gene develop a complex phenotype that is characterized by abnormal feeding behavior, progressive starvation, persistent hypoglycemia, hypotriglyceridemia, wasting, and neonatal mortality between days 2 and 14. Hypoglycemia in HNF-3alpha-null mice leads to physiological counter-regulatory responses in glucocorticoid and growth hormone production and an inhibition of insulin secretion but fails to stimulate glucagon secretion. Glucagon-producing pancreatic alpha cells develop normally in HNF-3alpha-/- mice, but proglucagon mRNA levels are reduced 50%. Furthermore, the transcriptional levels of neuropeptide Y are also significantly reduced shortly after birth, implying a direct role of HNF-3alpha in the expression of these genes. In contrast, mRNA levels were increased in HNF-3 target genes phosphofructo-2-kinase/fructose-2,6-bisphophatase, insulin growth factor binding protein-1, and hexokinase I of HNF-3alpha-null mice. Mice lacking one or both HNF-3alpha alleles also show impaired insulin secretion and glucose intolerance after an intraperitoneal glucose challenge, indicating that pancreatic beta-cell function is also compromised. Our results indicate that HNF-3alpha plays a critical role in the regulation of glucose homeostasis and in pancreatic islet function.
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PMID:Impaired glucose homeostasis and neonatal mortality in hepatocyte nuclear factor 3alpha-deficient mice. 1046 78