PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Skeletal muscle”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1995

Dexamethasone-induced changes in glucose transporter 4 in rat heart muscle, skeletal muscle and adipocytes.

To clarify the effect of glucocorticoid on glucose transporters (GLUT) in adipocytes and muscle, we examined the changes of GLUT4 in rat heart muscle, skeletal muscle and adipocytes during long-term administration of dexamethasone and the translocation of GLUT4. The levels of GLUT4 in the plasma membrane and the low-density microsome fraction were measured by Western blotting using anti-GLUT4 peptide antibody. The levels of GLUT4 in the heart and skeletal muscles of rat were unchanged by treatment of dexamethasone. In the adipocytes the level of GLUT4 in plasma membrane was changed, but it was decreased in the low-density microsome fraction. Although adipocytes are less involved in blood sugar regulation than skeletal muscle, this finding suggests that glucose metabolism in Cushing's syndrome is affected partly by a decrease of GLUT4 in the adipocytes.

5'-Nucleotidase↗
PubMed1976

Guanylate cyclase. Subcellular distribution in cardiac muscle, skeletal muscle, cerebral cortex and liver.

1. Guanylate cyclase of every fraction studied showed an absolute requirement for Mn2+ ions for optimal activity; with Mg2+ or Ca2+ reaction was barely detectable. Triton X-100 stimulated the particulate enzyme much more than the supernatant enzyme and solubilized the particulate-enzyme activity. 2. Substantial amounts of guanylate cyclase were recovered with the washed particulate fractions of cardiac muscle (63-98%), skeletal muscle (77-93%), cerebral cortex (62-88%) and liver (60-75%) of various species. The supernatants of these tissues contained 7-38% of total activities. In frog heart, the bulk of guanylate cyclase was present in the supernatant fluid. 3. Plasma-membrane fractions contained 26, 21, 22 and 40% respectively of the total homogenate guanylate cyclase activities present in skeletal muscle (rabbit), cardiac muscle (guinea pig), liver (rat) and cerebral cortex (rat). In each case, the specific activity of this enzyme in plasma membranes showed a five- to ten-fold enrichment when compared with homogenate specific activity. 4. These results suggest that guanylate cyclase, like adenylate cyclase, and ouabain-sensitive Na+ + K+-dependent ATPase (adenosine triphosphatase), is associated with the surface membranes of cardiac muscle, skeletal muscle, liver and cerebral cortex; however, considerable activities are also present in the supernatant fractions of these tissues which contain very little adenylate cyclase or ouabain-sensitive Na+ + K+-dependent ATPase activities.

Adenylyl Cyclases↗
PubMed1986

Effect of chronic exposure to static magnetic field upon the serum glutamic pyruvic transaminase activity GPT and morphology of the cardiac muscle, skeletal muscles, kidneys, cerebellum and lung tissue in guinea pigs.

In a cycle of investigations concerning the pathogenesis of functional changes caused by the influence of magnetic field of induction occurring in laboratory and industrial conditions glutamic pyruvic transaminase activity in external blood and morphological picture of cardiac muscle, skeletal muscles, kidneys, cerebellum and lung tissue in guinea pigs were examined. Static homogeneous magnetic field as low as 0.005 T produced a statistically significant decrease in GPT activity. The animals were exposed to the magnetic field action for seven weeks 1 hour a day, 7 days a week. The range of observed changes of enzyme activity were determined by the duration of magnetic field. No morphological changes were observed.

Alanine Transaminase↗
PubMed1980

Immunological differences between actins from cardiac muscle, skeletal muscle, and brain.

The antigenic similarities and differences between various actins were explored by use of antisera against purified bovine cardiac actin and chicken embryo brain actin. In double-antibody coprecipitation tests, purified iodinated actins from bovine cardiac muscle, rabbit skeletal muscle, chicken embryo brain, and bovine brain all bound to antiserum against chicken embryo brain actin. This result demonstrates the presence of shared antigenic determinants among these actins. Cardiac actin antiserum, on the other hand, bound cardiac and skeletal actin, but failed to bind significantly either brain actin. In radioimmunoassay, all four unlabeled actins were capable of some degree of inhibition of binding of (125)I-labeled chicken embryo brain actin to homologous antiserum. The results confirm the existence of shared or similar antigenic determinants, but also show that the molecules are not antigenically identical. In the cardiac actin radioimmunoassay, unlabeled cardiac and skeletal muscle actins inhibited the binding of (125)I-labeled cardiac actin to homologous antiserum, but neither brain actin inhibited the binding. Thus, the muscle actins possess at least one antigenic determinant not expressed by the brain actins, in addition to the shared determinants. Furthermore, cardiac actin and skeletal actin generated different inhibition curves in the cardiac actin radioimmunoassay, demonstrating that, although antigenically related, they are not identical. Correlations with existing sequence data imply that substitutions in only a few residues alter the antigenic properties of actin.

Actins↗
PubMed1978

Developmental changes in the activity of lipoprotein lipase (clearing-factor lipase) in rat lung, cardiac muscle, skeletal muscle and brown adipose tissue.

The lipoprotein lipase activity of the lung, skeletal muscle, heart muscle and brown adipose tissue of the rat was studied during the period from late foetal to adult life. The enzyme activity in all four tissues emerged substantially during the first 24th after birth. Subsequently, heart and lung enzyme activity remained relatively constant per unit wet weight of tissue. The enzyme activity present in brown adipose tissue and skeletal muscle was elevated per unit weight of tissue during suckling compared with other periods of life. Delivery of near-term foetuses stimulated the emergence of enzyme activity in all four tissues with the same time course as that evoked by normal delivery. The significance of the presence of the enzyme in the tissues and the activity changes which occurred during development are discussed in relation to possible mechanisms of control.

Adipose Tissue, Brown↗
PubMed1983

An X-linked mitochondrial disease affecting cardiac muscle, skeletal muscle and neutrophil leucocytes.

An X-linked recessive disease is reported in a large pedigree. The disease is characterised by a triad of dilated cardiomyopathy, neutropenia and skeletal myopathy. The untreated patients, all boys, died in infancy or early childhood from septicemia or cardiac decompensation. Ultrastructural abnormalities were observed in mitochondria in cardiac muscle cells, neutrophil bone marrow cells and to a lesser extent (0-9%) in skeletal muscle cells. Membrane-bound vacuoles were seen in neutrophil bone marrow cells. Intramuscular fat droplets were increased in type I skeletal muscle fibres. An affected patient had intermittent lactic acidemia, borderline low plasma carnitine, the latter decreasing during periods of illness, and low muscle carnitine (27% pretreatment; 35-40% posttreatment). While on treatment with oral carnitine he had less weakness and no cardiac complaints, but his neutropenia was not affected. Respiratory chain abnormalities were observed in this patient's isolated skeletal muscle mitochondria. These were: (1) diminished concentrations of cytochromes c1 + c, b and aa3 to 29, 47 and 64% of the averaged controls, and (2) a lowered P:0 ratio for oxidation of ascorbate + TMPD, with diminished uncoupler stimulated Mg2+-ATPase activity. Muscle AMP deaminase was deficient (5 resp. 17%). Only one previous report (Neustein et al. 1979) on X-linked mitochondrial cardiomyopathy exists, which probably refers to the same entity. Biochemical studies and haematological abnormalities (neutropenia) are reported for the first time.

Adenosine Triphosphatases↗
PubMed1976

Properties of particulate, membrane-associated and soluble guanylate cyclase from cardiac muscle, skeletal muscle, cerebral cortex and liver.

1. Guanylate cyclase of washed particles and plasma membranes showed S-shaped progress curves when titrated with either GTP or Mn2+ ions; similar results were obtained with Triton X-100-solubilized enzyme preparation from washed particles. Hill plots of these data revealed multiple metal-nucleotide and free-metal binding sites. 2. Guanylate cyclase of supernatant fractions displayed typical Michaelis-Menten properties when enzyme required excess of (free) Mn2+ (over GTP) for maximal activities; Ka (free Mn2+) was about 0.15-0.25 mM at subsaturating concentrations of GTP. 4 MnATP, MnADP, and MnGDP were found to increase the activities of both particulate and superantant enzyme, when MnGTP concentration was below saturation and free Mn2+ ion concentration was low (less than 100 muM); MnATP (50muM-1 mM) inhibited both these activities at high free Mn2+ concentration (1.5 mM) and inhibition of the particulate enzyme was greater than that of supernatant enzyme. 5. Ca2+ ions stimulated supernatant-enzyme activity; the stimulatory concentration of Ca2+ ions depended on the concentration of Mn2+ and GTP. 6. A modest stimulation of particulate guanylate cyclase by pyrophosphate (0.02-1 mM) was observed; the pyrophosphate effect appeared to be competitive with respect to GTP. At a higher concentration (2 mM), pyrophosphate produced a marked inhibition of particulate enzyme; the nature of inhibitory effect appeared complex. 7. Inorganic salts (e.g. NaCl, KCl, LiBr, NaF) produced inhibition of particulate enzyme; the degree of inhibition of Triton X-100-stimulated activity was less than that of unstimulated activity. 9. Treatment of sarcolemmal or microsomal membranes with either phospholipase C or trypsin decreased, whereas phospholipase A increased, the activity of guanylate cyclase.

Adenosine Triphosphate↗
PubMed1975

[New formation of the skeletal muscles and skeletal muscle and myocardial-like structures in rabbits in experiments with diffusion chambers].

The rabbit skeletal and cardiac muscles treated by 1% water solution of Trypan Blue for 48 hrs are necrotized and, having been transplanted under the skin in the diffusion chambers impermeable for cells, do not develop. When transplanting such necrotized muscles under the skin or in the abdominal cavity in the diffusion chambers permeable for cells (with pores of 1.5 mu in diameter), cells penetrate through the chamber wall and develop, under the influence of the products of decomposition of phagocytized transplant, into myoblasts, muscular tubes and differentiated cross-striated muscle fibers; undifferentiated muscle fibers of the skeletal type arise outside the chamber. The necrotized cardiac muscle did not induce the formation of muscle fibers after the transplantation under the skin or in the omentum. If they were transplanted together with the diffusion chambers containing the necrotized skeletal muscles, myocardium-like structures arose outside the chamber. The formation de novo of skeletal muscles and skeletal muscle- and myocardium-like structures under the influence of decomposition products released from the necrotized skeletal and cardiac muscles proceeds by means of induction; some pluripotent cells of the recipient, possibly polyblasts, are the source of de novo formation.

Animals↗
PubMed1986

Substrate regulation of the glucose transport system in rat skeletal muscle. Characterization and kinetic analysis in isolated soleus muscle and skeletal muscle cells in culture.

A self-regulatory mechanism of the glucose transport in rat skeletal muscle cells is described. In isolated rat soleus muscles and rat skeletal myocytes and myotubes in culture, pre-exposure to varying glucose concentrations modulated the rate of 2-deoxyglucose uptake. Maximal uptake was observed at glucose concentrations below 3 mM. Between 2.5 and 4.0 mM glucose it was reduced by 25-35%; further elevation of the glucose concentration resulted in a gradual decrease of the transport rate by approximately 2% for each millimolar glucose. The effect of glucose was time-dependent and fully reversible. Insulin rapidly increased the 2-deoxyglucose uptake in the soleus muscle; however, the insulin effect depended on the glucose concentration of the preincubation. Insulin was totally ineffective in muscles pre-exposed to 1.0-3.0 mM glucose, whereas its stimulatory action increased with increasing glucose concentrations above 4 mM. The effect of low glucose and insulin were not additive, and the maximal 2-deoxyglucose uptake rates induced by both conditions were of identical magnitude. It is postulated that glucose may "up- and down-regulate" its transport by affecting the number of active glucose transporters in the plasma membrane, and that insulin exerts its stimulatory effect only when the extracellular glucose reaches a threshold concentration.

Aminoisobutyric Acids↗
PubMed2004

Membrane traffic in skeletal muscle.

Skeletal muscle tissue is made up of highly organized multinuclear cells. The internal organization of the muscle cell is dictated by the necessary regular arrangement of repeated units within the protein myofibrils that mediate muscle contraction. Skeletal muscle cells have the usual membrane traffic pathways for partitioning newly synthesized proteins, internalizing cell surface receptors for hormones and nutrients, and mediating membrane repair. However, in muscle, these pathways must be further specialized to deal with targeting to and organizing muscle-specific membrane structures, satisfying the unique metabolic requirements of muscle and meeting the high demand for membrane repair in a tissue that is constantly under mechanical stress. Specialized membrane traffic pathways in muscle also play a role in the formation of muscle through fusion of myoblast membranes and the development of internal muscle-specific membrane structures during myogenesis and regeneration. It has recently become apparent that muscle-specific isoforms of proteins that are known to mediate ubiquitous membrane traffic pathways, as well as novel muscle-specific proteins, are involved in tissue-specific aspects of muscle membrane traffic. Here we describe the specialized membrane structures of skeletal muscle, how these are developed, maintained and repaired by specialized and generic membrane traffic pathways, and how defects in these pathways result in muscle disease.

Animals↗
PubMed2005

Effects of calcineurin activation on insulin-, AICAR- and contraction-induced glucose transport in skeletal muscle.

Skeletal muscle is composed of fast- and slow-twitch fibres with distinctive physiological and metabolic properties. The calmodulin-activated serine/threonine protein phosphatase calcineurin activates fast- to slow-twitch skeletal muscle remodelling through the induction of the slow-twitch skeletal muscle fibre gene expression programme, thereby enhancing insulin-stimulated glucose uptake and offering protection against dietary-induced insulin resistance. Given the profound influence of skeletal muscle fibre type on insulin-mediated responses, we determined whether the fast- to slow-twitch fibre-type transformation leads to alterations in insulin-independent glucose uptake in transgenic mice expressing a constitutively active form of calcineurin (MCK-CnA* mice). We determined whether skeletal muscle remodelling by activated calcineurin alters glucose transport in response to the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-beta-D-ribofuranoside (AICAR) or muscle contraction, two divergent insulin-independent activators of glucose transport. While insulin-stimulated glucose transport was increased 52%, the AICAR effect on glucose transport was 27% lower in MCK-CnA* mice versus wild-type mice (P < 0.05). In contrast, glucose transport was similar between genotypes after in vitro muscle contraction. Fibre-type transformation was associated with increased AMPKgamma1, decreased AMPKgamma3 and unchanged AMPKgamma2 protein expression between MCK-CnA* and wild-type mice (P < 0.05). The loss of AICAR-mediated glucose uptake is coupled to changes in the AMPK isoform expression, suggesting fibre-type dependence of the AICAR responses on glucose uptake. In conclusion, improvements in skeletal muscle glucose transport in response to calcineurin-induced muscle remodelling are limited to insulin action.

AMP-Activated Protein Kinases↗
PubMed2006

[The endocrine function of skeletal muscle].

Skeletal muscle has long been considered as an effector organ under the control of neural and humoral regulation. Recent studies indicated that skeletal muscle is not only an effector organ but also an endocrine organ. It is reported that the skeletal muscle can express, synthesis and secrete a lot of active factors, such as regulatory peptide, cytokine, growth factor and so on. The active factors play important roles not only in the growth, metabolism and motor function of skeletal muscle per se by paracrine/autocrine pathway but also in the function of peripheral tissues and organs by endocrine pathway. It is worthwhile to pay close attention to the significant effects of the skeletal muscle active factors on locomotor disease and some systemic diseases. This paper reviews the active factors secreted by skeletal muscles and their physiological and pathophysiological significance.

Cytokines↗
PubMed2003

The effect of hyperglycaemia on glucose disposal and insulin signal transduction in skeletal muscle.

Skeletal muscle is an important tissue for the proper maintenance of glucose homeostasis as it accounts for the major portion of glucose disposal following infusion or ingestion of glucose. Thus, cellular mechanisms regulating glucose uptake in skeletal muscle have a major impact on whole-body glucose homeostasis. Glucose transport into skeletal muscle is a rate-limiting step for glucose utilization under physiological conditions and a site of insulin resistance in patients with non-insulin-dependent diabetes mellitus (NIDDM). Defects in insulin signalling have been coupled to impaired glucose uptake in skeletal muscle from NIDDM patients. Although the exact aetiology is unclear, genetic and environmental (high-energy diets combined with a sedentary lifestyle) factors contribute to the onset of NIDDM. Furthermore, hyperglycaemia is linked with insulin resistance. This chapter will consider mechanisms for glucose disposal in skeletal muscle, potential sites of insulin resistance in skeletal muscle in NIDDM patients and the impact of hyperglycaemia on insulin action.

Animals↗
PubMed1996

Effects of thyroid hormones on contractility and cation transport in skeletal muscle.

Skeletal muscle is one of the major target organs for thyroid hormone. The muscles most commonly affected are those used during prolonged effort (slow-twitch muscles). One of the major clinical features is the shortening of the Achilles-tendon reflex time in hyperthyroidism and its prolongation in hypothyroidism. Most of the peripheral effects of the thyroid hormones can be ascribed to the action of triiodothyronine (T2), which is produced by de-iodination of thyroxine (T4) in liver and kidney. From the plasma, T3 is actively transported into skeletal muscle. The Ca2+ ATPase in skeletal muscle is responsible for removal of Ca2+ ions from the cytosol into the sarcoplasmic reticulum (SR) during relaxation, and the Na+, K+ ATPase in the plasma membrane is responsible for restoration of the membrane potential after excitation. The concentrations of Ca2+ ATPase and Na+, K+ ATPase in rat skeletal muscle have been shown to increase four- and 10-fold, respectively, in the transition from the hypothyroid to the hyperthyroid state. In humans, a linear correlation between the Na+, K+ ATPase concentration of skeletal muscle and the free T4 index was established. Significant effects of T3 on Ca2+ ATPase and Na+, K+ ATPase can be detected 24 h after a single injection. These effects are mediated by increased production of mRNA for the respective proteins, initiated by binding of T3 to nuclear receptors. Passive fluxes of Ca2+, Na+ and K+ also show a significant rise after T3 treatment. The increase in passive fluxes of Na+ and K+ can be detected before the rise in the concentration of Na+, K+ ATPase, suggesting that T3. In addition to its nuclear effects, may have a direct effect on the plasma membrane. Apart from their significance for muscle function in thyroid disease, the changes in Ca2+ ATPase and Na+, K+ ATPase will be important in other conditions where T3 and T4 levels show dramatic changes, i.e. during postnatal development, starvation and undernutrition, as well as in non-thyroidal illness (low-T3 syndrome).

Animals↗