scholarly journals Hypoxic Training Increases the Concentration of Serum Irisin and Reduces Weight in Diet-induced Obese Rats

2018 ◽  
Author(s):  
zhigang li ◽  
xiquan weng ◽  
Fangfang Zhao ◽  
Xue Song ◽  
Wentao Lin
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathway ◽  
Training Group ◽  
Treadmill Training ◽  
Exposure Group ◽  
Hypoxia Exposure ◽  
Hypoxic Training ◽  
Obese Rats ◽  
Group A ◽  
Oxygen Concentrations

Irisin promotes browning of white fat, improves energy metabolism, and weight loss. In this study, we investigated the effects of different oxygen concentrations during hypoxic training on the serum irisin and the PGC-1α(peroxisome proliferator-activated receptor gamma coactivator 1-alpha)-FNDC5(fibronectin type III domain containing 5)-UCP1(uncoupling protein 1) signaling pathway in the skeletal muscle of obese rats. Male Sprague-Dawley Obese rats (n=80) were randomly divided into 8 groups as follows: the control group (group A, n=10); the endurance exercise group (AE group, n=10), which involved animal treadmill training at slope 0°, 20 m/min, 40 min/d, and 5 d/w; the 16.3% hypoxia exposure group (group B, n=10), 13.3% hypoxia exposure group (group C, n=10), and 11.3% hypoxia exposure group (group D, n=10), which were exposed to a low oxygen environment with oxygen concentrations of 16.3%, 13.3%, and 11.3%, respectively, for 12 h/d; and the 16.3% hypoxic training group (BE group, n=10), 13.3% hypoxic training group (CE group, n=10), and 11.3% hypoxic training group (DE group, n=10) with animal treadmill training during hypoxia exposure. After 8 weeks, the serum irisin concentrations in the AE, BE, CE, and DE groups were significantly higher than that in the A group (p<0.05). Hypoxia exposure and hypoxic training at the three different concentrations significantly increased PGC-1α and FNDC5 gene expression in the skeletal muscle. The PGC-1α and FNDC5 protein contents were significantly higher in the skeletal muscle of the obese rats in the C, AE, and DE groups than those in group A (p<0.05). UCP1 protein expression was significantly higher in groups C, CE, D, and DE than in group A (p<0.05).To conclude, training at oxygen concentrations of 13.3% and 11.3% significantly increased the serum irisin level, and 11.3% hypoxic training enhanced the effects of the PGC-1α-Irisin-UCP1 signaling pathway in skeletal muscle.

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 PO-191 The effect of hypoxic training at different simulated altitude on the antioxidant activity mediated by Nrf2 in mice skeletal muscle

2018 ◽  
Vol 1 (4) ◽  
Author(s):  
Weixiu Ji ◽  
Ying Zhang
Keyword(s):  
Skeletal Muscle ◽  
Antioxidant Activity ◽  
Oxygen Concentration ◽  
Training Group ◽  
Control Group ◽  
Simulated Altitude ◽  
Wild Type ◽  
High Quality ◽  
Hypoxic Training ◽  
Nrf2 Protein

Objective It is generally believed that the long-term hypoxic training could impact oxidation resistance. Nrf2-Keapl signaling pathway is a key pathway of cell oxidative stress reaction. This research attempts to investigate the role and mechanism of Nrf2 in oxidation resistance to hypoxic training of different oxygen concentration. Methods Part one, 8-week-old Nrf2 knockout mice and wild type mice were divided into normoxic control group (NC), simulated altitude of 3500m hypoxic training group (3500HT) and simulated altitude of 5000m hypoxic training group (5000HT) randomly and respectively. The mice run on treadmill in speed of 12 m/min, 1h/day, 6day/week, for 4 weeks. Oxygen concentration in hypoxia was 13.3% and 10%. Mice were treated for 4 weeks, 8h/day. 48 h after the last training, the mice were sacrificed and skeletal muscles of legs were collected. Western Blot tested Nrf2 and antioxidant enzyme protein. Antioxidant enzymes mRNA were tested by RT-PCR. High quality fluorescence measurement was used to test ROS levels in skeletal muscle. Part two, The 30 C57BL/6J mice were divided into three groups: control group (WC), hypoxia group (WH), hypoxic training group (WHT). The hypoxic training arrangement was same as before. After both the interventions, the mice were sacrificed and collected skeletal muscle of legs. The expression of Nrf2, Keap1 and p-Nrf2 were analyzed by western blot. High quality fluorescence assay was done to detect ROS level in skeletal muscle of mice. Results (1) Compared with the same type mice NC group, Nrf2 protein, the mRNA and protein of CAT, GPX-1, GCLm, the mRNA of SOD1, SOD2, HO-1 were increased in wild type mice 3500HT group. And the Nrf2 protein, the mRNA and protein of SOD1, SOD2, the mRNA of CAT, NQO-1, GCLc, GCLm mRNA, the protein of HO-1 were decreased, and the ROS levels was higher in wile type mice 5000HT group. The mRNA of CAT, HO-1 in Nrf2-KO mice 3500HT group were increased, the mRNA and protein of SOD1, the mRNA of SOD2, the protein of GCLc were decreased, but the GCLc mRNA was increased in Nrf2-KO mice 5000HT group. When compared with the same intervention wild type mice, the mRNA and protein of SOD1, GPX-1, SOD2, HO-1, the mRNA of CAT, NQO-1, GCLc, GCLm were decreased in Nrf2-KO mice 3500HT group. The mRNA of GCLm, NQO-1, the protein of GCLc, HO-1 were decreased, but the GCLc mRNA was increased. (2) Nrf2/Keap1 complex contents in mice skeletal muscle of WH and WHT groups were significantly increased compared with WC group respectively. The free Nrf2 in mice skeletal muscle of WH、WHT groups were significantly reduced compared with WC group respectively. After both types of intervention, free Keap1 had no change nearly in skeletal muscle of mice. Compared with WC group, p-Nrf2 in mice skeletal muscle of WH and WHT groups were significantly reduced. The ROS level in mice skeletal muscle of WHT group significantly increased compared with WC group mice. Conclusions: Hypoxia and hypoxia training three interventions could increase Nrf2/Keap1 combination in skeletal muscle of mice, reduce the volume of free Nrf2; Phosphorylation of Nrf2 in skeletal muscle of mice in hypoxia training group was significantly lower, which may be result in marked increase in ROS level. Conclusions (1) Hypoxic training could affect antioxidant activity via Nrf2 in mice skeletal muscle, which is connected with the oxygen concentration. (2) Moderate hypoxia training (at the altitude of 3500m) can promote the antioxidant activity via Nrf2. However, extremely hypoxic training (at the altitude of 5000m) can restrain the antioxidant activity via Nrf2 through the inhibition of Nrf2/Keap1 dissociation.  

Differential effect of maturation on insulin- vs. contraction-stimulated glucose transport in Zucker rats

1995 ◽  
Vol 268 (6) ◽  
pp. E1154-E1160 ◽  
Author(s):  
P. L. Dolan ◽  
S. G. Boyd ◽  
G. L. Dohm
Keyword(s):  
Skeletal Muscle ◽  
Signaling Pathway ◽  
Glucose Transport ◽  
Insulin Signaling ◽  
Differential Effect ◽  
Glucose Transporter ◽  
Zucker Rats ◽  
Glut 4 ◽  
Obese Rats ◽  
Obese Male

Insulin-stimulated glucose transport has been shown to decline during maturation in lean rats. To determine whether this maturation-induced decrease occurred in the muscle of obese rats and whether the contraction-stimulated pathway for glucose transport was similarly affected, glucose transport rates were measured in insulin- and electrically stimulated skeletal muscle during hindlimb perfusion of 10- and 29-wk-old lean and obese male Zucker rats. Glucose transporter (GLUT-4) protein was also measured. Insulin-stimulated glucose transport rates were significantly decreased (36–56%) in 29-wk compared with 10-wk-old lean rats. There was no maturation-related decrease in GLUT-4. Insulin-mediated glucose transport was unaltered by maturation in skeletal muscle of obese rats. Differential effects of maturation on lean and obese rats caused the effect of obesity on maximally insulin-stimulated glucose transport to be much greater in 10- than 29-wk-old animals. Maturation had no effect on contraction-stimulated glucose transport rates in either lean or obese animals. The combined effect of maximal insulin plus contraction was not altered with maturity in lean animals but was significantly increased in 29- compared with 10-wk-old obese rats. Absence of a change in GLUT-4 content together with uncompromised contraction-stimulated glucose transport suggests that the maturation-induced decrease in insulin-stimulated glucose transport in lean rats is due to a defect in the insulin signaling pathway.

Adaptation to prolonged starvation in the rat: curtailment of skeletal muscle proteolysis

1981 ◽  
Vol 241 (4) ◽  
pp. E321-E327 ◽  
Author(s):  
M. N. Goodman ◽  
M. A. McElaney ◽  
N. B. Ruderman
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Early Event ◽  
Body Protein ◽  
Fed State ◽  
Prolonged Starvation ◽  
Obese Rats ◽  
Old Rats

Previous studies have established that 16-wk-old nonobese and obese rats conserve body protein during prolonged starvation. To determine the basis for this, protein synthesis and degradation in skeletal muscle were evaluated in the isolated perfused hindquarters of these rats, in the fed state and when starved for 2, 5, 10, and 11 days. Rats aged 4 and 8 wk were used as a comparison. The results indicate that the response to starvation depends on several factors: the age of the rat, its degree of adiposity, and the duration of the fast. An early event in starvation was a decline in muscle protein synthesis. This occurred in all groups, albeit this reduction occurred more slowly in the older rats. A later response to starvation was an increase in muscle proteolysis. This occurred between 2 and 5 days in the 8-wk-old rats. In 16-wk-old rats it did not occur until between 5 and 10 days, and it was preceded by a period of decreased proteolysis. In 16-wk-old obese rats, a decrease in proteolysis persisted for upwards of 10 days and the secondary increase was not noted during the period of study. The data suggest that the ability of older and more obese rats to conserve body protein during starvation is due, in part, to a curtailment of muscle proteolysis. This adaptation seems to correlate with the availability of lipid fuels.

Training-induced alterations of the in vivo force-velocity relationship of human muscle

1981 ◽  
Vol 51 (3) ◽  
pp. 750-754 ◽  
Author(s):  
V. J. Caiozzo ◽  
J. J. Perrine ◽  
V. R. Edgerton
Keyword(s):  
Training Group ◽  
Knee Extension ◽  
Knee Extensors ◽  
Velocity Relationship ◽  
Slow Velocity ◽  
Group A ◽  
Force Velocity ◽  
Group B ◽  
Relationship Of

Seventeen male and female subjects (ages 20–38 yr) were tested pre- and posttraining for maximal knee extension torque at seven specific velocities (0, 0.84, 1.68, 2.51, 3.35, 4.19, and 5.03 rad . s-1) with an isokinetic dynamometer. Maximal knee extension torques were recorded at a specific joint angle (0.52 rad below the horizontal plane) for all test speeds. Subjects were randomly assigned to one of three experimental groups: group A, control, n = 7; group B, training at 1.68 rad . s-1, n = 5; or group C, training at 4.19 rad . s-1, n = 5. Subjects trained the knee extensors by performing two sets of 10 single maximal voluntary efforts three times a week for 4 wk. Before training, each training group exhibited a leveling-off of muscular tension in the slow velocity-high force region of the in vivo force-velocity relationship. Training at 1.68 rad . s-1 resulted in significant (P less than 0.05) improvements at all velocities except for 5.03 rad . s-1 and markedly affected the leveling-off in the slow velocity-high force region. Training at 4.19 rad . s-1 did not affect the leveling-off phenomenon but brought about significant improvements (P less than 0.05) at velocities of 2.51, 3.35, and 4.19 rad . s-1. The changes seen in the leveling-off phenomenon suggest that training at 1.68 rad . s-1 might have brought about an enhancement of motoneuron activation.

Vitamin E prevents hypobaric hypoxia-induced mitochondrial dysfunction in skeletal muscle

2007 ◽  
Vol 113 (12) ◽  
pp. 459-466 ◽  
Author(s):  
José Magalhães ◽  
Rita Ferreira ◽  
Maria J. Neuparth ◽  
Paulo J. Oliveira ◽  
Franklim Marques ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vitamin E ◽  
Mitochondrial Dysfunction ◽  
Hypobaric Hypoxia ◽  
Mitochondrial Membrane ◽  
Mitochondrial Protein ◽  
Membrane Integrity ◽  
Outer Mitochondrial Membrane ◽  
Hypoxia Exposure

In the present study, the effect of vitamin E (α-tocopherol) on mice skeletal muscle mitochondrial dysfunction and oxidative damage induced by an in vivo acute and severe hypobaric hypoxic insult (48 h at a barometric pressure equivalent to 8500 m) has been investigated. Male mice (n=24) were randomly divided into the following four groups (n=6): control (C), hypoxia (H), vitamin E (VE; 60 mg/kg of body weight intraperitoneally, three times/week for 3 weeks) and hypoxia+VE (HVE). A significant increase in mitochondrial protein CGs (carbonyl groups) was found in the H group compared with the C group. Confirming previous observations from our group, hypoxia induced mitochondrial dysfunction, as identified by altered respiratory parameters. Hypoxia exposure increased Bax content and decreased the Bcl-2/Bax ratio, whereas Bcl-2 remained unchanged. Inner and outer mitochondrial membrane integrity were significantly affected by hypoxia exposure; however, vitamin E treatment attenuated the effect of hypoxia on mitochondrial oxidative phosphorylation and on the levels of CGs. Vitamin E supplementation also prevented the Bax and Bcl-2/Bax ratio impairments caused by hypoxia, as well as the decrease in inner and outer mitochondrial membrane integrity. In conclusion, the results suggest that vitamin E prevents the loss of mitochondrial integrity and function, as well as the increase in Bax content, which suggests that mitochondria are involved in increased cell death induced by severe hypobaric hypoxia in mice skeletal muscle.

14-Deoxy-11,12-Didehydroandrographolide Ameliorates Glucose Intolerance Enhancing the LKB1/AMPKα/TBC1D1/GLUT4 Signaling Pathway and Inducing GLUT4 Expression in Myotubes and Skeletal Muscle of Obese Mice

2021 ◽  
pp. 1-19
Author(s):  
Chih-Chieh Chen ◽  
Chong-Kuei Lii ◽  
Chia-Wen Lo ◽  
Yi-Hsueh Lin ◽  
Ya-Chen Yang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Time Dependent ◽  
Antidiabetic Activity ◽  
C2c12 Myotubes ◽  
Dependent Manner ◽  
Compound C

14-Deoxy-11,12-didehydroandrographolide (deAND), a bioactive component of Andrographis paniculata, has antidiabetic activity. AMP-activated protein kinase (AMPK) regulates glucose transport and ameliorates insulin resistance. The aim of the present study was to investigate whether activation of AMPK is involved in the mechanism by which deAND ameliorates insulin resistance in muscles. deAND amounts up to 40 [Formula: see text]M dose-dependently activated phosphorylation of AMPK[Formula: see text] and TBC1D1 in C2C12 myotubes. In addition, deAND significantly activated phosphorylation of LKB1 at 6 h after treatment, and this activation was maintained up to 48 h. deAND increased glucose uptake at 18 h after treatment, and this increase was time dependent up to 72 h. Compound C, an inhibitor of AMPK, suppressed deAND-induced phosphorylation of AMPK[Formula: see text] and TBC1D1 and reversed the effect on glucose uptake. In addition, the expression of GLUT4 mRNA and protein in C2C12 myotubes was up-regulated by deAND in a time-dependent manner. Promotion of GLUT4 gene transcription was verified by a pGL3-GLUT4 (837 bp) reporter assay. deAND also increased the nuclear translocation of MEF-2A and PPAR[Formula: see text]. After 16 weeks of feeding, the high-fat diet (HFD) inhibited phosphorylation of AMPK[Formula: see text] and TBC1D1 in skeletal muscle of obese C57BL/6JNarl mice, and deactivation of AMPK[Formula: see text] and TBC1D1 by the HFD was abolished by deAND supplementation. Supplementation with deAND significantly promoted membrane translocation of GLUT4 compared with the HFD group. Supplementation also significantly increased GLUT4 mRNA and protein expression in skeletal muscle compared with the HFD group. The hypoglycemic effects of deAND are likely associated with activation of the LKB1/AMPK[Formula: see text]/TBC1D1/GLUT4 signaling pathway and stimulation of MEF-2A- and PPAR[Formula: see text]-dependent GLUT4 gene expression, which account for the glucose uptake into skeletal muscle and lower blood glucose levels.

Effects of Quercetin and Coenzyme Q10 on Biochemical, Molecular, and Morphological Parameters of Skeletal Muscle in Trained Diabetic Rats

2021 ◽  
Vol 14 ◽  
Author(s):  
Amal M. Youssef ◽  
Dalia A. Mohamed ◽  
Samia Hussein ◽  
Doaa M. Abdullah ◽  
Shaimaa A. Abdelrahman
Keyword(s):  
Skeletal Muscle ◽  
Coenzyme Q10 ◽  
Combined Treatment ◽  
Diabetic Rats ◽  
Molecular Structures ◽  
Treadmill Training ◽  
Albino Rats ◽  
Musculoskeletal Function ◽  
Sugar Levels ◽  
Fibronectin Type Iii Domain

Background: Diabetes mellitus (DM) affects the musculoskeletal system through its metabolic perturbations. Exercise modulates blood sugar levels and increases the body’s sensitivity to insulin in patients with DM. Objective: This study aimed to investigate the potential effects of combined quercetin and coenzyme Q10 (CoQ10) supplements with or without exercise on the histological, biochemical and molecular structures of diabetic rat’s skeletal muscle. Method: A total of 64 adult male albino rats were divided into six groups: control, trained nondiabetic, non-trained diabetic, diabetic rats treated with combined CoQ10 and quercetin, diabetic rats with treadmill training, and diabetic rats treated with treadmill training and CoQ10 and quercetin. Blood and skeletal muscle samples were obtained from all groups for routine histological examination and biochemical determination of cytokine levels and protein activities. Quantitative real-time polymerase chain reaction (qRT-PCR) and morphometric analysis of PAS and Bax expressions were also performed. Results: Biochemical analysis revealed improvement in all studied parameters with combined CoQ10 and quercetin than exercise training alone. Combined treatment and exercise showed significant improvement in all parameters especially interleukin 6 and malondialdehyde. Fibronectin type III domain-containing protein 5 (FNDC5) expression and irisin levels increased in all trained groups but combined treatment with exercise significantly increased their levels than exercise alone. Histological analysis revealed improvement after exercise or combined treatment; however, when exercise was combined with CoQ10 and quercetin, marked improvement was observed. Conclusion: the combination of CoQ10 and quercetin could be promising in preserving musculoskeletal function in patients with DM concomitantly with physical exercise.

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