Academic literature on the topic 'L6 myotubes'
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Journal articles on the topic "L6 myotubes"
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Sultan, Karim R., Birgit Henkel, Maarten Terlou, and Henk P. Haagsman. "Quantification of hormone-induced atrophy of large myotubes from C2C12 and L6 cells: atrophy-inducible and atrophy-resistant C2C12 myotubes." American Journal of Physiology-Cell Physiology 290, no. 2 (February 2006): C650—C659. http://dx.doi.org/10.1152/ajpcell.00163.2005.
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Myofiber atrophy is the final outcome of muscle wasting induced by catabolic factors such as glucocorticoids and thyroid hormones. We set up an in vitro system to define the catabolic reaction based on myotube atrophy. Both mouse C2C12 and rat L6 cells were used. C2C12 myotube formation was improved by replacing horse serum with the serum substitute Ultroser G. A new method was developed to quantify size changes of large (0.5–1 mm) myotubes only, excluding remaining myoblasts and small myotubes. Dexamethasone reduced myotube size by 30% in L6 but not in C2C12 myotubes. Expression of the glucocorticoid receptor was twofold higher in L6 myotubes than in C2C12 myotubes. In both cell lines, 3,3′,5-triiodo-l-thyronine (T3) did not induce a significant size reduction. Expression of the major T3 receptor (T3Rβ1) was higher in L6 myotubes. We investigated whether the changes in myotube size are related to changes in atrogin-1 expression, as this enzyme is thought to be a key factor in the initiation of muscle atrophy. Dexamethasone induced a twofold increase of atrogin-1 mRNA; again, only L6 myotubes were susceptible. Interestingly, atrogin-1 expression in Ultroser G-fused C2C12 myotubes was lower than that in horse serum-fused myotubes. Furthermore, dexamethasone treatment increased atrogin-1 expression only in horse serum-fused myotubes but not in Ultroser G-fused myotubes. Ultroser G-induced fusion may result in atrophy-resistant C2C12 myotubes. Therefore, C2C12 myotubes offer an ideal system in which to study skeletal muscle atrophy because, depending on differentiation conditions, C2C12 cells produce atrophy-inducible and atrophy-resistant myotubes.
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Yang, H., J. M. Egan, Y. Wang, C. D. Moyes, J. Roth, M. H. Montrose, and C. Montrose-Rafizadeh. "GLP-1 action in L6 myotubes is via a receptor different from the pancreatic GLP-1 receptor." American Journal of Physiology-Cell Physiology 275, no. 3 (September 1, 1998): C675—C683. http://dx.doi.org/10.1152/ajpcell.1998.275.3.c675.
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The incretin hormone glucagon-like peptide-1 (GLP-1)-(7—36) amide is best known for its antidiabetogenic actions mediated via a GLP-1 receptor present on pancreatic endocrine cells. To investigate the molecular mechanisms of GLP-1 action in muscle, we used cultured L6 myotubes. In L6 myotubes, GLP-1 enhanced insulin-stimulated glycogen synthesis by 140% while stimulating CO2 production and lactate formation by 150%. In the presence of IBMX, GLP-1 diminished cAMP levels to 83% of IBMX alone. In L6 myotubes transfected with pancreatic GLP-1 receptor, GLP-1 increased cAMP levels and inhibited glycogen synthesis by 60%. An antagonist of pancreatic GLP-1 receptor, exendin-4-(9—39), inhibited GLP-1-mediated glycogen synthesis in GLP-1 receptor-transfected L6 myotubes. However, in parental L6 myotubes, exendin-4-(9—39) and GLP-1-(1—36) amide, an inactive peptide on pancreatic GLP-1 receptor, displaced125I-labeled GLP-1 binding and stimulated glycogen synthesis by 186 and 130%, respectively. These results suggest that the insulinomimetic effects of GLP-1 in L6 cells are likely to be mediated by a receptor that is different from the GLP-1 receptor found in the pancreas.
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Robinson, Matthew M., Bergen K. Sather, Emily R. Burney, Sarah E. Ehrlicher, Harrison D. Stierwalt, Maria Clara Franco, and Sean A. Newsom. "Robust intrinsic differences in mitochondrial respiration and H2O2 emission between L6 and C2C12 cells." American Journal of Physiology-Cell Physiology 317, no. 2 (August 1, 2019): C339—C347. http://dx.doi.org/10.1152/ajpcell.00343.2018.
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Rat L6 and mouse C2C12 cell lines are commonly used to investigate myocellular metabolism. Mitochondrial characteristics of these cell lines remain poorly understood despite mitochondria being implicated in the development of various metabolic diseases. To address this need, we performed high-resolution respirometry to determine rates of oxygen consumption and H2O2 emission in suspended myoblasts during multiple substrate-uncoupler-inhibitor titration protocols. The capacity for oxidative phosphorylation supported by glutamate and malate, with and without succinate, or supported by palmitoyl-l-carnitine was lower in L6 compared with C2C12 myoblasts (all P < 0.01 for L6 vs. C2C12). Conversely, H2O2 emission during oxidative phosphorylation was greater in L6 than C2C12 myoblasts ( P < 0.01 for L6 vs. C2C12). Induction of noncoupled respiration revealed a significantly greater electron transfer capacity in C2C12 compared with L6 myoblasts, regardless of the substrate(s) provided. Mitochondrial metabolism was also investigated in differentiated L6 and C2C12 myotubes. Basal rates of oxygen consumption were not different between intact, adherent L6, and C2C12 myotubes; however, noncoupled respiration was significantly lower in L6 compared with C2C12 myotubes ( P = 0.01). In summary, L6 myoblasts had lower respiration rates than C2C12 myoblasts, including lesser capacity for fatty acid oxidation and greater electron leak toward H2O2. L6 cells also retain a lower capacity for electron transfer compared with C2C12 following differentiation to form fused myotubes. Intrinsic differences in mitochondrial metabolism between these cell lines should be considered when modeling and investigating myocellular metabolism.
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Abdelmoez, Ahmed M., Laura Sardón Puig, Jonathon A. B. Smith, Brendan M. Gabriel, Mladen Savikj, Lucile Dollet, Alexander V. Chibalin, Anna Krook, Juleen R. Zierath, and Nicolas J. Pillon. "Comparative profiling of skeletal muscle models reveals heterogeneity of transcriptome and metabolism." American Journal of Physiology-Cell Physiology 318, no. 3 (March 1, 2020): C615—C626. http://dx.doi.org/10.1152/ajpcell.00540.2019.
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Rat L6, mouse C2C12, and primary human skeletal muscle cells (HSMCs) are commonly used to study biological processes in skeletal muscle, and experimental data on these models are abundant. However, consistently matched experimental data are scarce, and comparisons between the different cell types and adult tissue are problematic. We hypothesized that metabolic differences between these cellular models may be reflected at the mRNA level. Publicly available data sets were used to profile mRNA levels in myotubes and skeletal muscle tissues. L6, C2C12, and HSMC myotubes were assessed for proliferation, glucose uptake, glycogen synthesis, mitochondrial activity, and substrate oxidation, as well as the response to in vitro contraction. Transcriptomic profiling revealed that mRNA of genes coding for actin and myosin was enriched in C2C12, whereas L6 myotubes had the highest levels of genes encoding glucose transporters and the five complexes of the mitochondrial electron transport chain. Consistently, insulin-stimulated glucose uptake and oxidative capacity were greatest in L6 myotubes. Insulin-induced glycogen synthesis was highest in HSMCs, but C2C12 myotubes had higher baseline glucose oxidation. All models responded to electrical pulse stimulation-induced glucose uptake and gene expression but in a slightly different manner. Our analysis reveals a great degree of heterogeneity in the transcriptomic and metabolic profiles of L6, C2C12, or primary human myotubes. Based on these distinct signatures, we provide recommendations for the appropriate use of these models depending on scientific hypotheses and biological relevance.
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Rajesh, P., and K. Balasubramanian. "Di(2-ethylhexyl)phthalate exposure impairs insulin receptor and glucose transporter 4 gene expression in L6 myotubes." Human & Experimental Toxicology 33, no. 7 (October 15, 2013): 685–700. http://dx.doi.org/10.1177/0960327113506238.
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Di(2-ethyl hexyl)-phthalate (DEHP) is an endocrine disrupter and is the most abundantly used phthalate derivative, which is suspected to be an inevitable environmental exposure contributing to the increasing incidence of type-2 diabetes in humans. Therefore, the present study was designed to address the dose-dependent effects of DEHP on insulin signaling molecules in L6 myotubes. L6 myotubes were exposed to different concentrations (25, 50, and 100 μM) of DEHP for 24 h. At the end of exposure, cells were utilized for assessing various parameters. Insulin receptor and glucose transporter4 (GLUT4) gene expression, insulin receptor protein concentration, glucose uptake and oxidation, and enzymatic and nonenzymatic antioxidants were significantly reduced, but glutamine fructose-6-phosphate amidotransferase, nitric oxide, lipid peroxidation, and reactive oxygen species levels were elevated in a dose-dependent manner in L6 myotubes exposed to DEHP. The present study in turn shows the direct adverse effect of DEHP on the expression of insulin receptor and GLUT4 gene, glucose uptake, and oxidation in L6 myotubes suggesting that DEHP exposure may have a negative influence on insulin signaling.
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Sarabia, Vivian, Toolsie Ramlal, and Amira Klip. "Glucose uptake in human and animal muscle cells in culture." Biochemistry and Cell Biology 68, no. 2 (February 1, 1990): 536–42. http://dx.doi.org/10.1139/o90-076.
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Human muscle cells were grown in culture from satellite cells present in muscle biopsies and fusion-competent clones were identified. Hexose uptake was studied in fused myotubes of human muscle cells in culture and compared with hexose uptake in myotubes of the rat L6 and mouse C2C12 muscle cell lines. Uptake of 2-deoxyglucose was saturable and showed an apparent Km of about 1.5 mM in myotubes of all three cell types. The Vmax of uptake was about 6000 pmol/(min∙mg protein) in human cells, 4000 pmol/(min∙mg protein) in mouse C2C12 muscle cells, and 500 pmol/(min∙mg protein) in L6 cells. Hexose uptake was inhibited ~90% by cytochalasin B in human, rat, and mouse muscle cell cultures. Insulin stimulated 2-deoxyglucose uptake in all three cultures. The hormone also stimulated transport of 3-O-methylglucose. The sensitivity to insulin was higher in human and C2C12 mouse myotubes (half-maximal stimulation observed at 3.5 × 10−9 M) than in rat L6 myotubes (half-maximal stimulation observed at 2.5 × 10−8 M). However, insulin (10−6 M) stimulated hexose uptake to a larger extent (2.37-fold) in L6 than in either human (1.58-fold) or mouse (1.39-fold) myotubes. It is concluded that human muscle cells grown in culture display carrier-mediated glucose uptake, with qualitatively similar characteristics to those of other muscle cells, and that insulin stimulates hexose uptake in human cells. These cultures will be instrumental in the study of human insulin resistance and in investigations on the mechanism of action of antidiabetic drugs.Key words: glucose uptake, insulin action, primary muscle cultures, L6 cells, C2 cells.
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Ryu, Yunkyoung, Donghyen Lee, Seung Hyo Jung, Kyung-Jin Lee, Hengzhe Jin, Su Jung Kim, Hwan Myung Lee, Bokyung Kim, and Kyung-Jong Won. "Sabinene Prevents Skeletal Muscle Atrophy by Inhibiting the MAPK–MuRF-1 Pathway in Rats." International Journal of Molecular Sciences 20, no. 19 (October 8, 2019): 4955. http://dx.doi.org/10.3390/ijms20194955.
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Chrysanthemum boreale Makino essential oil (CBMEO) has diverse biological activities including a skin regenerating effect. However, its role in muscle atrophy remains unknown. This study explored the effects of CBMEO and its active ingredients on skeletal muscle atrophy using in vitro and in vivo models of muscle atrophy. CBMEO reversed the size decrease of L6 myoblasts under starvation. Among the eight monoterpene compounds of CBMEO without cytotoxicity for L6 cells, sabinene induced predominant recovery of reductions of myotube diameters under starvation. Sabinene diminished the elevated E3 ubiquitin ligase muscle ring-finger protein-1 (MuRF-1) expression and p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase1/2 (ERK1/2) phosphorylations in starved myotubes. Moreover, sabinene decreased the increased level of reactive oxygen species (ROS) in myotubes under starvation. The ROS inhibitor antagonized expression of MuRF-1 and phosphorylation of MAPKs, which were elevated in starved myotubes. In addition, levels of muscle fiber atrophy and MuRF-1 expression in gastrocnemius from fasted rats were reduced after administration of sabinene. These findings demonstrate that sabinene, a bioactive component from CBMEO, may attenuate skeletal muscle atrophy by regulating the activation mechanism of ROS-mediated MAPK/MuRF-1 pathways in starved myotubes, probably leading to the reverse of reduced muscle fiber size in fasted rats.
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Li, Yiming, Van H. Tran, Nooshin Koolaji, Colin Duke, and Basil D. Roufogalis. "(S)-[6]-Gingerol enhances glucose uptake in L6 myotubes by activation of AMPK in response to [Ca2+]i." Journal of Pharmacy & Pharmaceutical Sciences 16, no. 2 (July 10, 2013): 304. http://dx.doi.org/10.18433/j34g7p.
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PURPOSE. The aim of this study was to investigate the mechanism of (S)-[6]-gingerol in promoting glucose uptake in L6 skeletal muscle cells. METHODS. The effect of (S)-[6]-gingerol on glucose uptake in L6 myotubes was examined using 2-[1,2-3H]-deoxy-D-glucose. Intracellular Ca2+ concentration was measured using Fluo-4. Phosphorylation of AMPKα was determined by Western blotting analysis. RESULTS. (S)-[6]-Gingerol time-dependently enhanced glucose uptake in L6 myotubes. (S)-[6]-Gingerol elevated intracellular Ca2+ concentration and subsequently induced a dose- and time-dependent enhancement of threonine172 phosphorylated AMPKα in L6 myotubes via modulation by Ca2+/calmodulin-dependent protein kinase kinase. CONCLUSION. The results indicated that (S)-[6]-gingerol increased glucose uptake in L6 skeletal muscle cells by activating AMPK. (S)-[6]-gingerol, a major component of Zingiber officinale, may have potential for development as an antidiabetic agent. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.
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Fernandez, C., and R. D. Sainz. "Pathways of Protein Degradation in L6 Myotubes." Experimental Biology and Medicine 214, no. 3 (March 1, 1997): 242–47. http://dx.doi.org/10.3181/00379727-214-44092.
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Yonemitsu, S., H. Nishimura, M. Shintani, R. Inoue, Y. Yamamoto, H. Masuzaki, Y. Ogawa, et al. "Troglitazone Induces GLUT4 Translocation in L6 Myotubes." Diabetes 50, no. 5 (May 1, 2001): 1093–101. http://dx.doi.org/10.2337/diabetes.50.5.1093.
Full textDissertations / Theses on the topic "L6 myotubes"
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Yonemitsu, Shin. "Troglitazone induces GLUT4 translocation in L6 myotubes." Kyoto University, 2005. http://hdl.handle.net/2433/145305.
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Al-Abri, Abdulrahim. "Investigating the effect of PIP4K2a overexpression in insulin signalling in L6 myotubes." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-effect-of-pip4k2a-overexpression-in-insulin-signalling-in-l6-myotubes(1dd2d1dd-c765-4830-9b66-cf32a64d7de9).html.
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Insulin signalling is an essential process in humans by which the level of plasma glucose is maintained within the physiologically healthy range. Insulin activates the phosphoinositide 3 kinase (PI3K) signalling pathway that generates the phospholipid messenger PtdIns(3,4,5)P3, which in turn enhances the activity of two important proteins, AKT and Rac1. This then leads to increase the presence of the glucose transporter 4 (GLUT4) at the plasma membrane that enhances the intake of glucose, particularly in skeletal muscle cells and adipocytes. Insulin signalling also triggers interconversion of several other phosphoinositides (PIs) which play pivotal roles in different steps of glucose regulation. PtdIns5P is an important PI that is robustly increased after insulin treatment in the skeletal muscle cell line, L6 myotubes. Many of PtdIns5P`s functions are not fully understood. To gain more knowledge of the role of PtdIns5P in insulin signalling in muscle cells, the PtdIns5P kinase phosphatidylinositol-5-phosphate 4-kinase a (PIP4K2a) was over-expressed in L6 myotubes as a way of removing PtdIns5P, and the consequences in insulin signalling were studied. Although PtdIns5P is converted by PIP4K2a to PtdIns(4,5)P2 which is a precursor of the potent PI PtdIns(3,4,5)P3, previous studies revealed that the increase in PtdIns(3,4,5)P3 induced by insulin in control cells is diminished in cells overexpressing PIP4K2a, for unknown reasons. Additionally, although the phosphorylation of the serine/threonine protein kinase AKT was not affected in these L6 cells, glucose uptake was attenuated. The current study investigates the possible causes of attenuating glucose uptake in PIP4K overexpressing myotubes by examining the small GTPase Rac1 which plays an important role in the cytoskeleton re-arrangement that is necessary for GLUT4 translocation. Furthermore, the possible roles of PI phosphatases that may cause the disturbance on the levels of PIs in response to insulin were evaluated. Additionally, the potential role of PtdIns5P in Rac1 activation in L6 myotubes was further investigated by delivering synthetic PtdIns5P using a carrier-based delivery approach. The results showed that the attenuation of glucose uptake documented in previous studies occurred as a result of a defect in the process of translocating GLUT4 from intracellular storage to the plasma membrane. Rac1 activity was significantly reduced in cells expressing PIP4K2a. Quantifying the level of PIs suggested that PIP4K2a expression increases the removal of PtdIns(3,4,5)P3 by the PI 5-phosphatase, SKIP. Silencing the expression of SKIP by siRNA restored the level of PtdIns(3,4,5)P3 but Rac1 activity and the attenuation GLUT4 translocation were not rescued possibly as a result of removing PtdIns5P by PIP4K2a. On the other hand, exogenous delivery of PtdIns5P in L6 myotubes activates both Rac1 and GLUT4 translocation in the absence of insulin. However, activating GLUT4 translocation by the exogenous PtdIns5P requires PI3K activity since redistribution of GLUT4 to the plasma membrane is inhibited by the PI3K inhibitor, wortmannin. Removing PtdIns5P reduces Rac1 activity and stimulates SKIP that inhibits PtdIns(3,4,5)P3 increase which attenuates GLUT4 translocation and hence glucose uptake. These results emphasise the critical role played by PtdIns5P which seems to serve as a regulator of insulin signalling, both directly and/or by regulating other enzymes involved in the metabolism of PIs.
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Mohammed, Alisha. "Estrogen and progesterone alter glucose metabolism in L6 skeletal muscle myotubes while testosterone has no direct effect." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0021/MQ53352.pdf.
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Sishi, Balindiwe J. N. "An investigation into the P13-K/AKT signalling pathway in TNF-a-induced muscle proeolysis in L6 myotubes." Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/3039.
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Thesis (MSc (Physiological Sciences))--Stellenbosch University, 2008.Introduction: Skeletal muscle atrophy is a mitigating complication that is characterized by a reduction in muscle fibre cross-sectional area as well as protein content, reduced force, elevated fatigability and insulin resistance. It seems to be a highly ordered and regulated process and signs of this condition are often seen in inflammatory conditions such as cancer, AIDS, diabetes and chronic heart failure (CHF). It has long been understood that an imbalance between protein degradation (increase) and protein synthesis (decrease) both contribute to the overall loss of muscle protein. Although the triggers that cause atrophy are different, the loss of muscle mass in each case involves a common phenomenon that induces muscle proteolysis. It is becoming evident that interactions among known proteolytic systems (ubiquitin-proteosome) are actively involved in muscle proteolysis during atrophy. Factors such as TNF-α and ROS are elevated in a wide variety of chronic inflammatory diseases in which skeletal muscle proteolysis presents a lethal threat. There is an increasing body of evidence that implies TNF-α may play a critical role in skeletal muscle atrophy in a number of clinical settings but the mechanisms mediating its effects are not completely understood. It is also now apparent that the transcription factor NF-κB is a key intracellular signal transducer in muscle catabolic conditions. This study investigated the various proposed signalling pathways that are modulated by increasing levels of TNF-α in a skeletal muscle cell line, in order to synthesize our current understanding of the molecular regulation of muscle atrophy. Materials and Methods: L6 (rat skeletal muscle) cells were cultured under standard conditions where after reaching ± 60-65% confluency levels, differentiation was induced for a maximum of 8 days. During the last 2 days, myotubes were incubated with increasing concentrations of recombinant TNF-α (1, 3, 6 and 10 ng/ml) for a period of 40 minutes, 24 and 48 hours. The effects of TNF-α on proliferation and cell viability were measured by MTT assay and Trypan Blue exclusion technique. Morphological assessment of cell death was conducted using the Hoechst 33342 and Propidium Iodide staining method. Detection of apoptosis was assessed by DNA isolation and fragmentation assay. The HE stain was used for the measurement of cell size. In order to determine the source and amount of ROS production, MitoTracker Red CM-H2 X ROS was utilised. Ubiquitin expression was assessed by immunohistochemistry. PI3-K activity was calculated by using an ELISA assay and the expression of signalling proteins was analysed by Western Blotting using phospho-specific and total antibodies. Additionally, the antioxidant Oxiprovin was used to investigate the quantity of ROS production in TNF-α-induced muscle atrophy. Results and Discussion: Incubation of L6 myotubes with increasing concentrations of recombinant TNF-α revealed that the lower concentrations of TNF-α used were not toxic to the cells but data analysis of cell death showed that 10 ng/ml TNF-α induced apoptosis and necrosis. Long-term treatment with TNF-α resulted in an increase in the upregulation of TNF- α receptors, specifically TNF-R1. The transcription factors NF-κB and FKHR were rapidly activated thus resulting in the induction of the ubiquitin-proteosome pathway. Activation of this pathway produced significant increases in the expression of E3 ubiquitin ligases MuRF-1 and MAFbx. Muscle fibre diameter appeared to have decreased with increasing TNF-α concentrations in part due to the suppressed activity of the PI3-K/Akt pathway as well as significant reductions in differentiation markers. Western blot analysis also showed that certain MAPKs are activated in response to TNF-α. No profound changes were observed with ROS production. Finally, the use Oxiprovin significantly lowered cell viability and ROS production. These findings suggest that TNF-α may elicit strong catabolic effects on L6 myotubes in a dose and time dependent manner. Conclusion: These observations suggest that TNF-α might have beneficial effects in skeletal muscle in certain circumstances. This beneficial effect however is limited by several aspects which include the concentration of TNF-α, cell type, time of exposure, culture conditions, state of the cell (disturbed or normal) and the cells stage of differentiation. The effect of TNF-α can be positive or negative depending on the concentration and time points analysed. This action is mediated by various signal transduction pathways that are thought to cooperate with each other. More understanding of these pathways as well as their subsequent upstream and downstream constituents is obligatory to clarify the central mechanism/s that control physiological and pathophysiological effects of TNF-α in skeletal muscle.
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Singh, Indu, and indu singh@rmit edu au. "The influence of antioxidants on thrombotic risk factors in healthy population." RMIT University. Medical Sciences, 2008. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20081205.121719.
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Oxidative damage has been suggested to play a key role in the pathogenesis of atherosclerosis and other cardiovascular disease. Increased free radical production induced by oxidative stress can oxidise low density lipoproteins, activates platelets, induces endothelial dysfunction and disturbs glucose transport by consuming endogenous antioxidants. Using a combination, of in vitro and in vivo experimental models, the primary aims of the studies undertaken for this thesis were to examine whether different antioxidants could negate risk factors leading to thrombosis, atherosclerosis and other cardiovascular diseases. The studies utilised the mechanisms involved in platelet activity and glucose uptake by skeletal muscle myotubes. The first study determined if olive leaf extract would attenuate platelet activity in healthy human subjects. Blood samples (n=11) were treated with five different concentrations of extract of Olea europaea L. leaves ranging from 5.4£gg/mL to 54£gg/mL. A significant reduction in platelet activity (pless than0.001) and ATP release from platelets (p=0.02) was observed with 54£gg/mL olive leaf extract. The next crossover study compared the effect of exercise and antioxidant supplementation on platelet function between trained and sedentary individuals. An acute bout of 1 hour exercise (sub maximal cycling at 70% of VO2max) was used to induce oxidative stress in 8 trained and 8 sedentary male subjects, before and after one week supplementation with 236 mg/day of cocoa polyphenols. Baseline platelet count and ATP release increased significantly (pless than0.05) after exercise in all subjects. Baseline platelet numbers in the trained were higher than in the sedentary (235¡Ó37 vs. 208¡Ó34 x109/L, p less than 0.05), whereas platelet activation in trained subjects was lower than sedentary individuals (51¡Ó6 vs. 59¡Ó5%, p less than0.05). Seven days of cocoa polyphenol supplementation did not change platelet activity compared to the placebo group. The third study determined the effect of 5 weeks of either 100mg/day £^-Tocopherol (n=14), 200mg/d £^-Tocopherol (n=13) or placebo (n=12) on platelet function, lipid profile and the inflammatory marker C-reactive protein. Blood £^-tocopherol concentrations increased significantly (pless than0.05) relative to dose. Both doses attenuated platelet activation (pless than0.05). LDL cholesterol, platelet aggregation and mean platelet volume were decreased by 100mg/d £^-tocopherol (all pless than0.05). The final study determined the effect of glucose oxidase induced oxidative stress and £^-tocopherol treatment on glucose transport and insulin signalling in cultured rat L6 muscle cells. One hour treatment with 100mU/mL glucose oxidase significantly decreased glucose uptake both with and without 100nM insulin stimulation (pless than0.05). Pre-treatment with 100ÝM and 200ÝM £^-tocopherol partially protected cells from the effect of glucose oxidase, whereas 200ÝM £^-tocopherol restored both basal and insulin stimulated glucose transport to control levels. Glucose oxidase-induced oxidative stress did not impair basal or insulin stimulated phosphorylation of Akt or AS160, but 200ÝM £^-tocopherol improved insulin-stimulated phosphorylation of these proteins. In summary, the results from the studies undertaken for this thesis provide evidence that antioxidant supplementation maintains normal platelet function, exerts a positive effect on blood lipid profile and improves glucose uptake in normal healthy asymptomatic population as well as under conditions of induced oxidative stress. Antioxidants including foods rich in cocoa, olive and gamma tocopherol have the potential to combat oxidative stress induced risk factors leading to cardiovascular diseases.
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Hunnisett, Douglas J. "Leptin demonstrates no significant effect on basal or insulin-stimulated 2-deoxyglucose uptake and C¹§4-labelled glucose incorporation into glycogen in L6 myotubes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0024/MQ50346.pdf.
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YANG, XIAO YAN. "Effets de l'endotheline sur le calcium libre cytosolique et sur l'entree de glucose dans les myoblastes squelettiques humains en culture et dans les myotubes l6 : interet pour la comprehension de l'insuline-resistance." Paris 6, 1995. http://www.theses.fr/1995PA066779.
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Nous avons utilise l'endotheline comme outil pour approfondir le concept selon lequel certains agents vasoactifs, agissant par l'intermediaire de la mobilisation du ca#2#+ et de la stimulation de la proteine kinase c, peuvent agir sur les muscles squelettiques tissus-cibles de la resistance a l'insuline dans hypertension essentielle et modifier le transport du glucose dans ces cellules. D'une part, nous avons montre que les deux modeles choisis -les myoblastes squelettiques humains en culture provenant du vastus lateralis et les myotubes l6, une lignee de cellules musculaires squelettiques de rat- presentent deux sous-classes de recepteurs a l'endotheline, le type eta et le type etb. Le type eta est le recepteur predominant dans les cellules l6. Exposees a cette hormone, nos cellules subissent une tres forte augmentation du calcium libre cytosolique. Cet effet resulte de la mobilisation du ca#2#+ provenant des organelles intracellulaires. D'autre part, nous avons detecte, dans les myoblastes squelettiques humains en culture, l'expression des deux isotypes du transporteur de glucose: le glut-1 present dans la plupart des tissus, et le glut-4 exprime dans les tissus sensibles a l'insuline. Apres avoir verifie que l'insuline augmente l'entree de #3h-deoxy-d-glucose dans nos cellules, le resultat le plus interessant de notre etude est que l'endotheline est egalement capable de stimuler cette entree. L'effet de ce dernier sur l'entree de #3h-deoxy-glucose n'est pas additif a celui de l'insuline. De plus, l'entree de #3h-deoxy-glucose peut etre augmentee par un traitement avec du 12-myristate 13-acetate phorbol, un activateur de la proteine kinase c. L'augmentation de l'entree de #3h-deoxy-d-glucose mediee par l'endotheline et l'insuline est totalement abolie par la calphostine c, un inhibiteur specifique de la proteine kinase c. Ceci suggere que l'augmentation de l'entree de glucose sous l'effet de l'endotheline et de l'insuline, dans les muscles squelettiques humains, fait intervenir des mecanismes dependant, au moins partiellement, de la proteine kinase c. L'angiotensine ii presente un effet similaire a celui de l'endotheline sur le profil du calcium libre cytosolique, mais cet agent est incapable de modifier l'entree de 2-deoxy-d-glucose. Il est donc tres probable que l'alteration du metabolisme du glucose induit par l'endotheline n'est pas liee directement a l'augmentation du calcium cytosolique. En conclusion, des conditions associees a l'augmentation des niveaux d'endotheline ou d'agents similaires a proximite des muscles squelettiques pourraient modifier la reponse de ce tissu a l'insuline. Par consequent, des niveaux augmentes d'endotheline dans le lit vasculaire pourraient contribuer a alterer le metabolisme du glucose dans l'hypertension essentielle, via les muscles squelettiques, et par la meme expliquer pourquoi certains patients hypertendus presentent une diminution de la sensibilite a l'insuline
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Brunetti, Donato. "The characterization of the glucose tolerance factor (GTF) in L6 myotubes and 3T3-L1 adipocytes." Thesis, 2004. http://spectrum.library.concordia.ca/8338/1/MR04338.pdf.
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This thesis reports the effects of the Glucose Tolerance Factor (GTF) on the stimulation of 2-deoxyglucose (2-DG) transport in 3T3-L1 adipocytes and in L6 myotubes. The maximal effects on 2-DG transport in adipocytes were observed at concentrations of 133 nM insulin. The maximal effect of GTF was seen at 20 mg/ml in 3T3-L1 fat cells while maximal stimulation of GTF was seen in L6 myotubes at 50 mg/ml. These observations indicated that GTF had similar effects to insulin in stimulating glucose uptake in 3T3-L1 adipocytes and in L6 myotubes. Also, GTF works in an additive manner with insulin giving a higher stimulation in glucose transport without interfering with insulin binding to its receptor. GTF's mode of action is not through the phosphorylation of the insulin receptor β chain. However, GTF seems to stimulate phosphorylation of downstream signals such as the IRS-1. (Abstract shortened by UMI.)
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Chou, Yi-Chun, and 周怡君. "Effect and Mechanisms of Momordica charantia Extract on Glucose Uptake in 3T3-L1 Adipocytes and L6 Myotubes." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/49982884700275344702.
Full textAbstract:
碩士國立臺灣大學
生化科技學系
99
Bitter gourd (Momordica Charantia, BG) is a common tropical vegetable that has also been used in traditional medicine for treating diabetes. Numerous research in past decades have provided evidences supporint the hypoglycemic effect of BG. Insulin like polypeptide-p and triterpenoids from BG have been demonstrated for their hypoglycemic effect in vivo and in vitro. This study aims at examing the effects of BG water extract and its feactions on the glucose uptake of 3T3-L1 adipocytes and L6 myotute. Lyophilized powder of wild bitter gourd (Hualian NO.4) was extracted with water (WE), treated with enzyme and extracted with ethyl acetate(We-E), and butanol (We-B). Small molecular weight fraction of WE (WES) was treated similarly and give rise to fractions Se-E and Se-B. Insulin-like peptide fraction (Pf) was isolated from WE. Cells, treated with various BG samples for 30min or 12 hr, were examined for their 3H-labeled 2-deoxyglucose uptake at basal or palmitate-induced insulin resistant state and in the presence or presence of insulin. In 3T3-L1 adipocytes, WE, WES, Se-E and Pf were increased glucose uptake in both basal and insulin resistant state (p<0.05), and also improved insulin resistance and amplified insulin action. Associated with these effects, 3T3-L1 adipocytes treated with BG WE and fractions for 12hr showed enhanced Akt phosphorylation, detected by western-blot analysis. In L6 myotubes, We-E, Se-E, and Pf increased glucose uptake after 30min treatment. Myotubes treated with Se-E for 12 hrs also showed higher glucose uptake. Most importantly, all BG samples prevented palmitate-induced inhibition of glucose uptake. These datas suggested that the wild bitter gourd contains hypoglycemic components wihich increased adipocytes and myptubes uptake glucose. Among our BG fraction, Se-E might be the most effective fraction.
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Lin, Jia-Wei, and 林家暐. "An initial approach to explore the effects of Momordica chanratia L. extracts on mitochondrial biogenesis and functions in L6 and C2C12 myotubes." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/96914360024778540706.
Full textBooks on the topic "L6 myotubes"
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Mohammed, Alisha. Estrogen and progesterone alter glucose metabolism in L6 skeletal muscle myotubes while testosterone has no direct effect. Ottawa: National Library of Canada, 2000.
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Hunnisett, Douglas J. Leptin demonstrates no significant effect on basal or insulin-stimulated 2-deoxyglucose uptake and C14-labelled glucose incorporation into glycogen in L6 myotubes. Ottawa: National Library of Canada, 2000.
Find full textBook chapters on the topic "L6 myotubes"
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Cheong, Sun Hee, and Kyung Ja Chang. "Antidiabetic Effect of Taurine in Cultured Rat Skeletal L6 Myotubes." In Advances in Experimental Medicine and Biology, 311–20. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6130-2_26.
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Dang, Nhung Thuy, Masanori Yamaguchi, Tadashi Yoshida, Ken-ichi Yoshida, and Hitoshi Ashida. "Insulin-Mimetic Activity of Inositol Derivatives Depends on Phosphorylation of PKCζ/λ in L6 Myotubes." In Basic and Applied Aspects, 327–31. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3892-0_54.
Full textConference papers on the topic "L6 myotubes"
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Gong, Longlong, Lei Liu, and Da Xing. "Low-Power Laser Irradiation Promotes Reactive Oxygen Species Production in L6 Myotubes." In Asia Communications and Photonics Conference. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/acpc.2016.af2a.40.
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Hanbing Li, Jing Nie, and Yunxue Pan. "Astragaloside IV improved insulin resistance in L6 myotubes induced by high glucose and insulin." In 2011 International Conference on Remote Sensing, Environment and Transportation Engineering (RSETE). IEEE, 2011. http://dx.doi.org/10.1109/rsete.2011.5966083.
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