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Muscle Level (muscle + level)
Selected AbstractsSeasonally changing metabolism in Atlantic salmon (Salmo salar L.) II ,, -oxidation capacity and fatty acid composition in muscle tissues and plasma lipoproteinsAQUACULTURE NUTRITION, Issue 5 2003U. Nordgarden Abstract With the aim of elucidating seasonally changing lipid metabolism in immature Atlantic salmon (Salmo salar L.) in sea water, one group was reared under simulated natural light, while one group was reared under continuous light. Fatty acid profile in plasma lipoproteins did not vary during the experiment, while , -oxidation capacity increased during spring, concurrent with decreasing temperatures. Simultaneously, the relative level of monounsaturated fatty acids (MUFA) in muscle tissue decreased (42,36%). Muscle levels of saturated fatty acids were low during early spring (19%), but then increased slowly, and muscle levels of polyunsaturated fatty acids increased during spring (from 36% to 39%). It is suggested that increased spring growth and the concomitant energy demand was met by increased lipid oxidation, where MUFA were preferred as energy substrate. [source] Plasticity of human skeletal muscle: gene expression to in vivo functionEXPERIMENTAL PHYSIOLOGY, Issue 5 2007Stephen D. R. Harridge Human skeletal muscle is a highly heterogeneous tissue, able to adapt to the different challenges that may be placed upon it. When overloaded, a muscle adapts by increasing its size and strength through satellite-cell-mediated mechanisms, whereby protein synthesis is increased and new nuclei are added to maintain the myonuclear domain. This process is regulated by an array of mechanical, hormonal and nutritional signals. Growth factors, such as insulin-like growth factor I (IGF-I) and testosterone, are potent anabolic agents, whilst myostatin acts as a negative regulator of muscle mass. Insulin-like growth factor I is unique in being able to stimulate both the proliferation and the differentiation of satellite cells and works as part of an important local repair and adaptive mechanism. Speed of movement, as characterized by maximal velocity of shortening (Vmax), is regulated primarily by the isoform of myosin heavy chain (MHC) contained within a muscle fibre. Human fibres can express three MHCs: MHC-I, -IIa and -IIx, in order of increasing Vmax and maximal power output. Training studies suggest that there is a subtle interplay between the MHC-IIa and -IIx isoforms, with the latter being downregulated by activity and upregulated by inactivity. However, switching between the two main isoforms appears to require significant challenges to a muscle. Upregulation of fast gene programs is caused by prolonged disuse, whilst upregulation of slow gene programs appears to require significant and prolonged activity. The potential mechanisms by which alterations in muscle composition are mediated are discussed. The implications in terms of contractile function of altering muscle phenotype are discussed from the single fibre to the whole muscle level. [source] Myotonic dystrophy 1 in the nervous system: From the clinic to molecular mechanismsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2008Mario Bermúdez de León Abstract Myotonic dystrophy type 1 (DM1) is a dominant neuromuscular disorder caused by the expansion of trinucleotide CTG repeats in the 3,-untranslated region (3,-UTR) of the DMPK gene. Prominent features of classical DM1 are muscle wasting and myotonia, whereas mental retardation is distinctive for congenital DM1. The main nervous system symptoms of DM1 are cognitive impairment, neuroendocrine dysfunction, and personality and behavior abnormalities. It is thought that expansion of CTG repeats causes DM1 pathology through different molecular mechanisms; however, a growing body of evidence indicates that an RNA gain-of-function mechanism plays a major role in the disease development. At the skeletal muscle level, three main molecular events can be distinguished in this model: 1) formation of nuclear foci that are composed at least of mutant DMPK mRNA and recruited RNA-binding proteins, such as splicing regulators and transcription factors; 2) disturbance of alternative splicing of specific genes; and 3) impairment of cell differentiation. Contrasting with the substantial advances in understanding DM1 muscle pathology, the molecular basis of DM1 in the nervous system has just started to be revealed. This review focuses in the DM1 nervous system pathology and provides an overview of the genetic and molecular studies analyzing the effects of the DMPK gene CUG expanded repeats on cell function in neuronal systems. A comparison between the molecular mechanisms of DM1 in the skeletal muscle and those identified in DM1 nervous system models is provided. Finally, future directions in the study of DM1 in the nervous system are discussed. © 2007 Wiley-Liss, Inc. [source] Inclusion of macroalgae meal (Macrocystis pyrifera) as feed ingredient for rainbow trout (Oncorhynchus mykiss): effect on flesh fatty acid compositionAQUACULTURE RESEARCH, Issue 1 2009Patricio Dantagnan Abstract The use of macroalgae as an additional component in animal feeding has been studied. However, information on how it could influence muscle composition of fish body is scarce. This study evaluates four diets with different macroalgae inclusion levels (0%, 1.5%, 3% and 6%) to test the effect on body fatty acid composition of rainbow trout. Tanks with a volume of 600 L were stocked with 60.6 ± 7.9 g fish at a density of 45 individuals tank,1 and fed for 124 days. At the end of the experiment there were not significant differences (P<0.05) in muscle proximate composition among fish fed the different treatments. However, it was determined that inclusion of 3% and 6% of macroalgae meal resulted in a significant increase (P<0.05) of polyunsaturated fatty acids (PUFAs) in muscle. In summary, macroalgae meal in rainbow trout diets do not enhance the quantity of protein and lipid contents at muscle level but an addition of 3,6% might contribute to increase the level of PUFAs, specially EPA, DHA and LIN. Thus, use of macroalgae meal might help to increase lipid quality content in the final product due the beneficial effects of PUFAs for human health. [source] Pharmacokinetics of oxolinic acid in gilthead sea bream, Sparus aurata L.JOURNAL OF FISH DISEASES, Issue 7 2002G Rigos This is the first study on the pharmacokinetic parameters of oxolinic acid (OA) in gilthead sea bream, Sparus aurata L. The kinetic profile of OA was studied after a single intravascular injection (20 mg kg,1) in 100 g fish at 20 °C. The distribution half-life (t1/2,) and the elimination half-life (t1/2,) of the drug were found to be short (0.51 and 12.60 h, respectively). The drug penetration from the plasma to the tissues was adequate as the apparent volume of distribution of the drug at steady-state (Vd(ss)) was found to be 2.11 L kg,1. The mean residence time (MRT) of OA was short (14.25 h) and the total clearance rate (ClT) of the drug was low (0.15 L kg,1 h,1). The bioavailability (F,%) of OA following oral administration (30 mg kg,1) was also low (14%). Maximum values were observed for muscle at 0.5 h after injection, with levels declining as with subsequent sampling. At the first two time points (0.5 and 1 h) plasma levels of OA were higher than muscle, however, the reverse was evident for subsequent samples. Following oral administration, highest muscle levels were found at 16 h and, with the exception of the 24-h sampling, muscle OA concentrations were higher than plasma at all time points. The fast elimination of OA suggests short withdrawal times with reference to human consumption of treated fish. [source] Angiotensin II Is a Critical Mediator of Prazosin-Induced Angiogenesis in Skeletal MuscleMICROCIRCULATION, Issue 6 2007Matthew C. Petersen ABSTRACT Objective: The purpose of this study was to determine whether a high-salt diet modulates physiological angiogenesis in skeletal muscle by altering angiotensin II (ANGII) and vascular endothelial growth factor (VEGF) levels. Methods: Sprague-Dawley rats were placed on a control diet (0.4% NaCl by weight) or high-salt diet (4.0% NaCl) prior to treatment with the vasodilator prazosin in the drinking water. In addition, a group of animals fed high salt were infused intravenously with ANGII at a low dose to prevent ANGII suppression by high salt, and a group of rats fed control diet were treated with the angiotensin II type I (AT1) receptor blocker losartan and prazosin. Results: Prazosin induced significant angiogenesis in the tibialis anterior muscle after 1 week of treatment. High-salt-fed rats demonstrated a complete inhibition of this angiogenic response. Maintenance of ANGII levels restored prazosin-induced angiogenesis in animals fed a high-salt diet. In addition, losartan treatment blocked prazosin-induced angiogenesis in animals on a control diet. Western blot analysis indicated that prazosin-induced angiogenesis was independent of changes in muscle levels of VEGF. Conclusions: This study demonstrates an inhibitory effect of high salt intake on prazosin-induced angiogenesis. Further, these results indicate that ANGII acting through the AT1 receptor is a critical pathway in this model of angiogenesis. [source] Seasonally changing metabolism in Atlantic salmon (Salmo salar L.) II ,, -oxidation capacity and fatty acid composition in muscle tissues and plasma lipoproteinsAQUACULTURE NUTRITION, Issue 5 2003U. Nordgarden Abstract With the aim of elucidating seasonally changing lipid metabolism in immature Atlantic salmon (Salmo salar L.) in sea water, one group was reared under simulated natural light, while one group was reared under continuous light. Fatty acid profile in plasma lipoproteins did not vary during the experiment, while , -oxidation capacity increased during spring, concurrent with decreasing temperatures. Simultaneously, the relative level of monounsaturated fatty acids (MUFA) in muscle tissue decreased (42,36%). Muscle levels of saturated fatty acids were low during early spring (19%), but then increased slowly, and muscle levels of polyunsaturated fatty acids increased during spring (from 36% to 39%). It is suggested that increased spring growth and the concomitant energy demand was met by increased lipid oxidation, where MUFA were preferred as energy substrate. [source] | |||||||||||||