scholarly journals PO-204 Effects of hypoxia and/or endurance exercise on autophagy of skeletal muscle in rats with nutritional obesity

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Fangfang Zhao ◽  
Wentao Lin ◽  
跟 Wen
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Blood Lipids ◽  
Muscle Cells ◽  
Exercise Group ◽  
The Body ◽  
Skeletal Muscle Cells ◽  
High Fat ◽  
Group A ◽  
Group D

  Objective The globalization of obesity has become an important factor threatening human health, and the rational health of the solution has driven the exploration of experts and scholars. For this reason, this experiment uses hypoxia and exercise as interventions for 8 weeks. Changes of autophagy-related factors LC3 mRNA, p62 mRNA and energy regulation factor AMPKα2 mRNA, and cell stress-inducing factor Sestrin2 mRNA after hypoxia and/or combined endurance exercise, and explored the effect of hypoxia endurance exercise on autophagy of skeletal muscle cells To provide a reasonable experimental basis for exploring hypoxic exercise to lose weight and to prevent or reduce autophagy-related diseases. Methods  First, a nutritional obese rat model fed with high-fat diet for 8 weeks was constructed and randomly divided into 8 groups: the normoxia group (A), the normoxic group (AE), and 16.3%. Oxygen quiet group (B) and 16.3% hypoxic exercise group (BE), 13.3% hypoxic quiet group (C), 13.3% hypoxic exercise group (CE), 11.3% hypoxic quiet group (D), 11.3% low Oxygen exercise group (DE), 10 in each group, and continued to feed with high fat diet. Secondly, establish a hypoxic and/or endurance exercise model, and the experimental experiment is expected. The rat training program is as follows: the normoxia quiet group does not perform any endurance exercise and other interventions under normoxia; the normoxic exercise group is large. The rats underwent a medium-intensity endurance exercise with a running speed of 20 m/min in a normal oxygen environment for 40 min. Similarly, rats in the hypoxic quiet group underwent continuous hypoxia intervention for 12h in the corresponding hypoxic environment; the hypoxic-binding endurance exercise group was based on the intervention of the hypoxic-quiet group, with a time of 40 min and a running speed of 20 m/ Min's medium-intensity endurance exercise. The frequency of exercise is 5 times a week (every Monday to Friday) for 8 weeks. After the last training, fasting for 24 hours, the rats were sacrificed and sampled. Biochemical indicators were used to measure blood lipids and blood glucose concentration; real-time quantitative PCR was used to detect the expression of autophagy regulators Sestrin2, AMPKɑ2 and autophagy Beclin1 and LC3II mRNA. Results 1.Nutritional obesity rat model: After 8 weeks of high-fat feeding, the body weight, Lee's index, BG, TC, TG and LDL-c concentrations in the high-fat group were significantly increased (P<0.05) 2.Changes in morphology and blood lipids of rats: Compared with group A, the body weight, BG, TC, TG, LDL-c concentrations in the AE group were significantly decreased (P<0.05), and the HDL-c concentration was significantly increased (P<0.05). LDL-c in group D, TG and BD concentrations in group B, group C and group D were significantly decreased (P<0.05), and HDL-c concentrations in groups C and D were significantly increased (P<0.05); Compared with the group, the LDL-c and TG concentrations in the DE group were significantly lower (P<0.05), the BG concentrations in the CE group and the DE group were significantly lower (P<0.05), and the HDL-c concentration in the DE group was significantly increased (P<0.05). ). 3.Real-time quantitative PCR showed that compared with group A, the expression of Sestrin2, Beclin1 and LC3II mRNA in skeletal muscle cells of AE group, C group and D group was significantly increased (P<0.05), and the expression of AMPKɑ2 mRNA in group D was significantly increased. Compared with AE group, the expressions of Beclin1, LC3II and AMPKɑ2 mRNA in CE group and DE group were significantly increased (P<0.05), and the expression of Sestrin2 mRNA in DE group was significantly increased (P<0.05). Conclusions   1.Three different concentrations of hypoxia and / or combined endurance exercise can reduce the body weight of obese rats, improve the blood sugar, blood lipids, hypoxia and exercise in obese rats, the effect of weight loss, blood sugar and blood lipids is more obvious. 2.Endurance exercise, hypoxic exposure, hypoxia combined with endurance exercise can induce autophagy in skeletal muscle cells; and the cumulative stimulation effect of exercise and hypoxia is more prominent than simple endurance exercise and hypoxia exposure. 3.Three different concentrations of hypoxia and/or combined endurance exercise can up-regulate the expression of Sestrin2, AMPKɑ2, Beclin1, and LC3II mRNA, thereby effectively activating and enhancing the autophagy level of skeletal muscle cells in obese rats, especially 11.3% hypoxia. The endurance exercise group has a more pronounced effect.

scholarly journals PO-212 Effects of hypoxic endurance training on weight loss and Irisin expression in nutritional obese rats

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Zhigang Li ◽  
Wentao Lin
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Oxygen Concentration ◽  
Training Group ◽  
The Body ◽  
Hypoxia Exposure ◽  
Obese Rats ◽  
Group A ◽  
Group B ◽  
Group D

Objective Exercise can induce the release of various myokine such as Irisin, which promote browning of white fat, improve body metabolism, and loss weight. Appropriate hypoxic training plays a better role in weight loss than single exercise, but the effect of hypoxic training on muscle factors that promote browning of fat is rarely reported. Therefore, this study aims to observe different concentrations of hypoxia training on the PGC1α-Irisin-UCP1 signaling pathway in nutritional obese rats, and the role of weight loss. Methods Male Sprague-Dawley rats (n=140) of 6 weeks old were divided into normal diet feeding group (group N, n=20) and high-fat diet feeding group (group HFD, n=120). The HFD rats became obese after 8 weeks’ feeding, and they were further divided randomly into 8 groups. Including sedentary group(group A), training group (group AE), 16.3% hypoxia exposure group (group B), 16.3% hypoxia training group (group BE), and 13.3% hypoxia exposure group (group C), 13.3% hypoxia training group (group CE), 11.3% hypoxia exposure group (group D), 11.3% hypoxia training group (group DE), group B, group C and group D Rats were exposed to oxygen in concentrations of 16.3%, 13.3%, and 11.3% for 12 h/d, respectively. Rats in group BE, CE, and DE were subjected to animal treadmill training during hypoxic exposure with a slope of 0°, 20 m /min, 40min/d, 5d/w. After 8 weeks of intervention, blood, adipose tissue and skeletal muscle were collected and tested. Results (1) In group AE, the body weight of obese rats decreased in a short time, but bounced back later. The body weight of rats in group CE and group DE decreased continuously. Hypoxia exposure and hypoxia training can inhibit the food intake of obese rats in varying degrees, and group CE has the most obvious effect. Hypoxia, endurance training and hypoxia training all reduced the percentage of visceral fat to body weight, group C is significantly lower than group B and D group (p < 0.05), the effect of hypoxia training is more obvious than single hypoxia or exercise, and the lower oxygen concentration the more significant effect. Group C、group CE、group D and group DE significantly decreased the concentration of LDL-C, increased the content of HDL-C in serum than other groups (p < 0.05).(2) The concentration of serum Irisin in group AE, group BE, group CE and group DE rats was significantly higher than that in group A (p < 0.05), and the highest level was found in group CE and DE. The insulin resistance of obese rats in group CE and group DE was significantly better than that in group AE (p < 0.05). (3) Three different concentrations of hypoxia exposure and hypoxia training can significantly increase the skeletal muscle PGC-1 α and FNDC5 gene expression, showing that the lower the concentration of oxygen, the higher the expression, 13.3% and 16.3% hypoxia training can significantly promote the gene transcription of UCP1. The contents of PGC-1 α and FNDC5 protein in skeletal muscle of obese rats in group C, AE and DE were significantly higher than those in group A (p < 0. 05). The expression of UCP1 protein in skeletal muscle of rats in group C, CE and DE was significantly higher than that in group A (p < 0. 05). Conclusions 13.3% and 11.3% oxygen concentration combined with endurance training can effectively reduce the body weight and visceral fat of nutritional obese rats, enhance serum HDL-C and decrease LDL-C levels and insulin resistance. 13.3% and 11.3% oxygen concentration training can significantly improve the level of serum Irisin, 11.3% oxygen concentration training can significantly promote the expression of PGC1α-Irisin-UCP1 gene and protein in skeletal muscle.

scholarly journals Exercise improves lipid metabolism disorders induced by high-fat diet in a SESN2/JNK- independent manner

2021 ◽  
Author(s):  
Tianyi Wang ◽  
Wenqing Hu ◽  
Yanmei Niu ◽  
Sujuan Liu ◽  
Li Fu
Keyword(s):  
Skeletal Muscle ◽  
Lipid Metabolism ◽  
High Fat Diet ◽  
Muscle Cells ◽  
Vital Role ◽  
Lipid Biosynthesis ◽  
Skeletal Muscle Cells ◽  
High Fat ◽  
Jnk Signaling ◽  
Lipid Disorder

SESN2 and JNK are emerging powerful stress-inducible proteins in regulating lipid metabolism. The aim of this study was to determine the underlying mechanism of SESN2/JNK signaling in exercise improving lipid disorder induced by high-fat diet (HFD). Our data showed that HFD and SESN2 knockout resulted in abnormalities including elevated body weight, increased fat mass, serum total cholesterol (TC), lipid biosynthesis related proteins, and a concomitant increase of pJNK-Thr183/Tyr185. The above changes were reversed by exercise training. SESN2 silencing or JNK inhibition in palmitate-treated C2C12 further confirmed that SESN2 and JNK play a vital role in lipid biosynthesis. Rescue experiment further demonstrated that SESN2 reduced lipid biosynthesis through inhibition of JNK. SESN2/JNK signaling axis regulates lipid biosynthesis in both animal and cell models with abnormalities of lipid metabolism induced by HFD or palmitate treatment. This study provided evidence that exercise ameliorated lipid metabolic disorder induced by HFD feeding or by SESN2 knockout. SESN2 may improve lipid metabolism through inhibition JNK expression in skeletal muscle cells, providing a molecular mechanism that may represent an attractive target for the treatment of lipid disorder. Novelty: ● Exercise improved lipid disorder induced by HFD feeding and SESN2 knockout. ● SESN2 and JNK play a vital role in lipid biosynthesis in vivo and in vitro. ● SESN2 suppressed JNK to improve lipid metabolism in skeletal muscle cells.

Fiber type conversion alters inactivation of voltage-dependent sodium currents in murine C2C12skeletal muscle cells

2004 ◽  
Vol 287 (2) ◽  
pp. C270-C280 ◽  
Author(s):  
Eva Zebedin ◽  
Walter Sandtner ◽  
Stefan Galler ◽  
Julia Szendroedi ◽  
Herwig Just ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fiber Type ◽  
Muscle Fibers ◽  
Muscle Cells ◽  
The Body ◽  
Skeletal Muscle Cells ◽  
Prolonged Treatment ◽  
Type Conversion ◽  
Electrophysiological Properties ◽  
Slow Fiber

Each skeletal muscle of the body contains a unique composition of “fast” and “slow” muscle fibers, each of which is specialized for certain challenges. This composition is not static, and the muscle fibers are capable of adapting their molecular composition by altered gene expression (i.e., fiber type conversion). Whereas changes in the expression of contractile proteins and metabolic enzymes in the course of fiber type conversion are well described, little is known about possible adaptations in the electrophysiological properties of skeletal muscle cells. Such adaptations may involve changes in the expression and/or function of ion channels. In this study, we investigated the effects of fast-to-slow fiber type conversion on currents via voltage-gated Na+channels in the C2C12murine skeletal muscle cell line. Prolonged treatment of cells with 25 nM of the Ca2+ionophore A-23187 caused a significant shift in myosin heavy chain isoform expression from the fast toward the slow isoform, indicating fast-to-slow fiber type conversion. Moreover, Na+current inactivation was significantly altered. Slow inactivation less strongly inhibited the Na+currents of fast-to-slow fiber type-converted cells. Compared with control cells, the Na+currents of converted cells were more resistant to block by tetrodotoxin, suggesting enhanced relative expression of the cardiac Na+channel isoform Nav1.5 compared with the skeletal muscle isoform Nav1.4. These results imply that fast-to-slow fiber type conversion of skeletal muscle cells involves functional adaptation of their electrophysiological properties.

Factors Controlling Movement of Skeletal Muscles

Leonardo ◽  
2015 ◽  
Vol 48 (3) ◽  
pp. 270-271
Author(s):  
Miranda D. Grounds
Keyword(s):  
Skeletal Muscle ◽  
Extracellular Matrix ◽  
Cell Membrane ◽  
Skeletal Muscles ◽  
Muscle Cells ◽  
The Body ◽  
Skeletal Muscle Cells ◽  
3 Dimensional

The contraction of specialized skeletal muscle cells results in classic movements of bones and other parts of the body that are vital for life. There is exquisite control over the movement of diverse types of muscles. This paper indicates the way in which skeletal muscles (myofibres) are formed; then factors that contribute to generating the movement are outlined: these include the nerve, sarcomeres, cytoskeleton, cell membrane and the extracellular matrix. The factors controlling the movement of mature myofibres in 3-dimensional tissues in vivo are vastly more complex than for tissue cultured immature muscle cells in an artificial in vitro environment.

Cinnamomum cassiaPrevents High-Fat Diet-Induced Obesity in Mice through the Increase of Muscle Energy

2017 ◽  
Vol 45 (05) ◽  
pp. 1017-1031 ◽  
Author(s):  
Mi Young Song ◽  
Seok Yong Kang ◽  
Anna Kang ◽  
Ji Hye Hwang ◽  
Yong-Ki Park ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Biogenesis ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Obese Mouse ◽  
Oral Glucose ◽  
Obese Mice ◽  
High Fat

The cortex of Cinnamomum cassia Presl (Cinnamomi Cortex: CC) has commonly been used for weight control in traditional medicines, but without a scientific basis. Therefore, this study was undertaken to investigate the anti-obesity effect of CC extract in a high-fat diet (HFD)-induced obese mouse model and in C2C12 mouse skeletal muscle cells. Male C57BL/6 mice were fed a normal diet or a HFD for 16 consecutive weeks, and orally administered CC extract (100 or 300[Formula: see text]mg/kg) or metformin (250[Formula: see text]mg/kg; positive control) daily for 16 weeks. CC extract administration significantly decreased body weights, food intakes, and serum levels of glucose, insulin, total cholesterol and ALT levels, prevented oral glucose tolerance and insulin resistance, inhibited the protein expressions of MyHC and PGC1[Formula: see text] and the phosphorylation of AMPK, suppressed lipid accumulation in liver, decreased adipocyte size and increased muscle mass in obese mice. For this in vitro study, C2C12 myoblasts were differentiated into the myotubes for five days, and then treated with CC extract (0.1 or 0.2[Formula: see text]mg/ml) for 24[Formula: see text]h. CC extract significantly increased ATP levels by increasing the mRNA expressions of mitochondrial biogenesis-related factors, such as, PGC1[Formula: see text], NRF-1, and Tfam, and the phosphorylations of AMPK and ACC. Our results suggest CC extract controls weight gain in obese mice by inhibiting lipid accumulation and increasing energy expenditure, and that its action mechanism involves the up-regulation of mitochondrial biogenesis in skeletal muscle cells.

scholarly journals Glucocorticoid Receptor Alpha Targets SLC2A4 to Regulate Protein Synthesis and Breakdown in Porcine Skeletal Muscle Cells

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 721
Author(s):  
Xiao-Li Du ◽  
Wei-Jing Xu ◽  
Jia-Li Shi ◽  
Kai Guo ◽  
Chang-Tong Guo ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Cells ◽  
The Body ◽  
Skeletal Muscle Cells ◽  
Luciferase Reporter ◽  
Protein Breakdown ◽  
Reporter Assays ◽  
Solute Carrier ◽  
Regulate Protein ◽  
Hpa Axis Activity

In the presence of stress, the hypothalamic-pituitary-adrenal (HPA) axis activity can be enhanced to promote the secretion of a large amount of glucocorticoids (GCs), which play an important role in the anabolism and catabolism of skeletal muscle. When the endogenous and exogenous glucocorticoids are deficient or excessive, the body will produce stress-related resistance and change the protein metabolism. In this study, we investigated the effect of GC receptor GRα on protein breakdown and synthesis in porcine skeletal muscle cells (PSCs). Overexpression of GRα was shown to increase the expression of protein degradation-related genes, while knockdown of GRα decreased the expression of these genes. Additionally, we found a relationship between GRα and solute carrier family 2 member 4 (SLC2A4), SLC2A4 expression level increases when stress occurs, suggesting that increasing SLC2A4 expression can partially alleviate stress-induced damage, and we found that there is a combination between them via luciferase reporter assays, which still needs to be confirmed in further studies.

scholarly journals The Zinc Transporter Zip7 Is Downregulated in Skeletal Muscle of Insulin-Resistant Cells and in Mice Fed a High-Fat Diet

Cells ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 663 ◽  
Author(s):  
Shaghayegh Norouzi ◽  
John Adulcikas ◽  
Darren Henstridge ◽  
Sabrina Sonda ◽  
Sukhwinder Sohal ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Metabolism ◽  
Cell Signaling ◽  
Insulin Signaling ◽  
High Fat Diet ◽  
Muscle Cells ◽  
Zinc Transporter ◽  
Skeletal Muscle Cells ◽  
High Fat ◽  
Insulin Resistant

Background: The zinc transporter Zip7 modulates zinc flux and controls cell signaling molecules associated with glucose metabolism in skeletal muscle. The present study evaluated the role of Zip7 in cell signaling pathways involved in insulin-resistant skeletal muscle and mice fed a high-fat diet. Methods: Insulin-resistant skeletal muscle cells were prepared by treatment with an inhibitor of the insulin receptor, HNMPA-(AM)3 or palmitate, and Zip7 was analyzed along with pAkt, pTyrosine and Glut4. Similarly, mice fed normal chow (NC) or a high-fat diet (HFD) were also analyzed for protein expression of Glut4 and Zip7. An overexpression system for Zip7 was utilized to determine the action of this zinc transporter on several genes implicated in insulin signaling and glucose control. Results: We identified that Zip7 is upregulated by glucose in normal skeletal muscle cells and downregulated in insulin-resistant skeletal muscle. We also observed (as expected) a decrease in pAkt and Glut4 in the insulin-resistant skeletal muscle cells. The overexpression of Zip7 in skeletal muscle cells led to the modulation of key genes involved in the insulin signaling axis and glucose metabolism including Akt3, Dok2, Fos, Hras, Kras, Nos2, Pck2, and Pparg. In an in vivo mouse model, we identified a reduction in Glut4 and Zip7 in the skeletal muscle of mice fed a HFD compared to NC controls. Conclusions: These data suggest that Zip7 plays a role in skeletal muscle insulin signaling and is downregulated in an insulin-resistant, and HFD state. Understanding the molecular mechanisms of Zip7 action will provide novel opportunities to target this transporter therapeutically for the treatment of insulin resistance and type 2 diabetes.

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