Muscle Of Obese Rats Research Articles

Protective Role of Ovothiol-A against Muscle and Kidney Injuries in Obese Rats

Background: Obesity is a serious chronic metabolic disease impairing health damaging many organs such as kidneys and muscles. Ovothiol-A (Ovo-A) has been found to keep the redox balance normal in sea urchins indicating its antioxidant characteristics. Aim: This study aims to investigate the protective effects of Ovo-A on kidneys and muscles in obese rats. objective: Investigation of the protective effect of Ovo-A on kidneys and muscles in obese rats. Methods: In-silco studies were performed on lactate dehydrogenase (LDH) and creatine kinase (CK) with Ovo-A to compute their binding affinities. Obesity was induced by high-fat diet (HFD) for 4 weeks. Wistar rats were used in this study as 6 rats per group as control, HFD, Ovo-A (200 and 400 mg/Kg, p.o) groups. Results: Docking results have revealed that Ovo-A has affinities to bind to LDH (-8.5 kcal/mol) and CK (-17.7 kcal/mol). Ovo-A reduced the levels of uric acid, urea, creatinine, LDH, CK, malondialdehyde (MDA), and nitric oxide (NO), while increasing the levels of glutathione (GSH), catalase (CAT), and glutathione-S-transferase (GST). Histopathological investigations have revealed that Ovo-A restored the renal and muscular structure. Conclusion: The current study showed that Ovo-A has a protective effect on kidneys and muscles in obese rats. Ovo-A enhances renal and muscular functions by inhibiting LDH and CK activities and improving the antioxidant system. Ovo-A is more effective in the high dose.

Sa1943 MECHANOKINETICS OF MUSCLE FATIGUE DEVELOPMENT IN SOLEUS MUSCLES OF OBESE RATS

Sa1943 MECHANOKINETICS OF MUSCLE FATIGUE DEVELOPMENT IN SOLEUS MUSCLES OF OBESE RATS

MiR-122/PPARβ axis is involved in hypoxic exercise and modulates fatty acid metabolism in skeletal muscle of obese rats

Hypoxic exercise is an effective intervention for obesity, because it promotes weight loss by regulating fatty acid (FA) metabolism. The regulation of peroxisome proliferator-activated receptor β (PPARβ) by miR-122 may be involved in this process, but the detailed mechanisms are unknown. In order to address this issue, we probed how miR-122 affected the expression of factors associated with FA metabolism in skeletal muscle of obese rats undergoing hypoxic training. By injecting adeno-associated virus 9 containing miR-122 overexpression vector or miR-122 inhibitor into skeletal muscles of rats with a 4-week hypoxic exercise regimen, the miR-122 expression level can be regulated. Body composition and blood lipid levels were analyzed, and PPARβ, carnitine palmitoyltransferase 1b (CPT1b), acetylCoA carboxylase 2 (ACC2), and FA synthase (FAS) mRNA and protein levels were evaluated using quantitative reverse transcription quantitative PCR(RT-qPCR) and Western blot analysis. We found that miR-122 overexpression increased low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG) levels and decreased PPARβ, ACC2, and FAS expression. Conversely, miR-122 inhibition decreased TG level, increased high-density lipoprotein cholesterol (HDL-C) level, and upregulated PPARβ, ACC2, FAS, and CPT1b. These data indicated that the negative regulation of PPARβ by miR-122 promotes FA metabolism by altering the levels of the factors related to FA metabolism in skeletal muscle of obese rat under hypoxic training, thus providing molecular-level insight into the beneficial effects of this intervention.

The effect of aerobic training and hydroalcoholic extract of dill on skeletal muscle inflammation in a high-fat diet-induced obesity rat model

Abstract Aerobic training (AT) and herbal medicine interventions are effective in reducing chronic inflammation and achieving weight loss. The present study aimed to investigate the effect of 10 weeks of AT and hydroalcoholic extract of dill (HED) on tumour necrosis factor-alpha (TNF-α), interleukin-4 (IL-4), and peroxisome proliferator-activated receptor gamma (PPARγ) concentrations in gastrocnemius muscle and Lee index of obese male rats. Thirty-two obese male Wistar rats were randomly divided into AT (70-80% of maximal oxygen uptake, 5 times/week), HED (300 mg/kg body weight, 3 times/week), AT+HED, and obese control (Ctr), and eight non-obese rats were included in the non-obese control group (NCtr). Lee index was measured before and after 10 weeks of interventions. Also, rats were sacrificed 48 hs after the last intervention session and gastrocnemius muscle was removed to measure protein concentrations of TNF-α, IL-4, and PPARγ. When compared with the pre-intervention period, the Lee index decreased in the AT and AT+HED groups and increased in the NCtr group at the post-intervention period. Also, there was no significant difference between non-obese and obese rats in the concentrations of TNF-α and IL-4, but the AT+HED group showed a higher concentration of TNF-α than the AT group. Furthermore, the expression of PPARγ protein in the HED group was higher than in the Ctr and AT groups. Although we observed the beneficial effects of AT and its combination with HED in reducing the Lee index, we found that the administration of HED compared with AT can provide better protection against some metabolic complications in the skeletal muscles of obese rats caused by a high-fat diet. Lastly, it seems that the AT combined with HED interferes with possible anti-inflammatory effects of AT or HED intervention alone.

AGE AND OBESITY INTERFERES IN MUSCLE HYPERTROPHY IN RATS UNDERGOING HIIT TRAINING

Sarcopenic obesity is a condition characterized by the simultaneous presence of obesity andsarcopenia, which is the loss of muscle mass and function. Is a growing concern, especiallyamong the elderly population, and it is important to address both obesity and sarcopeniathrough lifestyle modifications, such as exercise and proper nutrition, to improve overallhealth and quality of life. Our study aimed to evaluate the effect of HIIT training on themuscle fiber area of the EDL muscle in obese rats of different ages. For that, Wistar rats, 7and 12 months old, submitted or not to a HFD diet were subjected to HIIT training, 3 times aweek, on alternate days, for 8 consecutive weeks. After the euthanasia EDL muscles wascollected and processed histologically. Our data showed that HIIT training was able topromote muscle hypertrophy even with consumption of this diet, indicating that practicingthis exercise can stimulate protein synthesis even under conditions of obesity.

Acute effects of a single moderate-intensity exercise bout performed in fast or fed states on cell metabolism and signaling: Comparison between lean and obese rats

AimsAlthough the benefits of exercise can be potentiated by fasting in healthy subjects, few studies evaluated the effects of this intervention on the metabolism of obese subjects. This study investigated the immediate effects of a single moderate-intensity exercise bout performed in fast or fed states on the metabolism of gastrocnemius and soleus of lean and obese rats. Main methodsMale rats received a high-fat diet (HFD) for twelve weeks to induce obesity or were fed standard diet (SD). After this period, the animals were subdivided in groups: fed and rest (FER), fed and exercise (30 min treadmill, FEE), 8 h fasted and rest (FAR) and fasted and exercise (FAE). Muscle samples were used to investigate the oxidative capacity and gene expression of AMPK, PGC1α, SIRT1, HSF1 and HSP70. Key findingsIn relation to lean animals, obese animals' gastrocnemius glycogen decreased 60 %, triglycerides increased 31 %; glucose and alanine oxidation decreased 26 % and 38 %, respectively; in soleus, triglycerides reduced 46 % and glucose oxidation decreased 37 %. Exercise and fasting induced different effects in glycolytic and oxidative muscles of obese rats. In soleus, fasting exercise spared glycogen and increased palmitate oxidation, while in gastrocnemius, glucose oxidation increased. In obese animals' gastrocnemius, AMPK expression decreased 29 % and SIRT1 increased 28 % in relation to lean. The AMPK response was more sensitive to exercise and fasting in lean than obese rats. SignificanceExercise and fasting induced different effects on the metabolism of glycolytic and oxidative muscles of obese rats that can promote health benefits in these animals.

Naringin Ameliorates Skeletal Muscle Atrophy and Improves Insulin Resistance in High-Fat-Diet-Induced Insulin Resistance in Obese Rats.

Obesity causes progressive lipid accumulation and insulin resistance within muscle cells and affects skeletal muscle fibres and muscle mass that demonstrates atrophy and dysfunction. This study investigated the effects of naringin on the metabolic processes of skeletal muscle in obese rats. Male Sprague Dawley rats were divided into five groups: the control group with normal diet and the obese groups, which were induced with a high-fat diet (HFD) for the first 4 weeks and then treated with 40 mg/kg of simvastatin and 50 and 100 mg/kg of naringin from week 4 to 8. The naringin-treated group showed reduced body weight, biochemical parameters, and the mRNA expressions of protein degradation. Moreover, increased levels of antioxidant enzymes, glycogen, glucose uptake, the expression of the insulin receptor substrate 1 (IRS-1), the glucose transporter type 4 (GLUT4), and the mRNA expressions of protein synthesis led to improved muscle mass in the naringin-treated groups. The in vitro part showed the inhibitory effects of naringin on digestive enzymes related to lipid and glucose homeostasis. This study demonstrates the potential benefits of naringin as a supplement for treating muscle abnormalities in obese rats by modulating the antioxidative status, regulating protein metabolism, and improved insulin resistance in skeletal muscle of HFD-induced insulin resistance in obese rats.

Comparative Effect of Three Different Exercise Intensities in Combination with Diazoxide on Contraction Capacity and Oxidative Stress of Skeletal Muscle in Obese Rats

Simple SummaryObesity is a growing public health problem worldwide. It is a pathological state that degrades the proper functioning of skeletal muscle. Diazoxide treatment and exercise have been shown to generally improve muscle function. However, the effect that each of the different exercise intensities has when combined with diazoxide on the contraction capacity, resistance to fatigue and oxidative stress levels in rat skeletal muscle is unknown. Therefore, this work focused on analyzing which exercise intensity was more efficient in combination with diazoxide in improving muscle tissue and its metabolic capacities. The best results were obtained with low- and moderate-intensity exercise when combined with the drug. These results expected to open a window of time that allows the implementation of a constant and prolonged exercise protocol that completely reverses the harmful effects of obesity on muscle tissue and obesity itself.Obesity is a chronic disease that impairs skeletal muscle function, affects the ability to contract, and promotes the development of fatigue. For this reason, the study of treatments that seek to reduce the harmful effects of obesity on muscle tissue has been deepened. Diazoxide treatment and various exercise protocols have been proposed to protect skeletal muscle against oxidative stress and its effects. However, the intensity and duration of exercise combined with diazoxide that would obtain the best results for improving skeletal muscle function in obese rats is unknown. To this end, this study evaluated the effects of three different exercise intensities combined with diazoxide on contraction capacity, resistance to fatigue, markers of oxidative stress, lipid peroxidation, ROS, and glutathione redox status of skeletal muscle. The results showed that treatments with diazoxide and exercise at different intensities improved muscle contraction capacity by reducing oxidative stress during obesity, with the best results being obtained with low-intensity exercise in combination with diazoxide. Therefore, these results suggest that diazoxide and low-intensity exercise improve muscle function during obesity by decreasing oxidative stress with the same efficiency as a moderate-intensity exercise protocol.

Effect of high-intensity interval training and coenzyme Q10 supplementation on cardiac apoptosis in obese male rats.

Obesity is associated with several metabolic disorders and myocardial apoptosis. The aim of this study was to determine the effect of high-intensity interval training (HIIT) and coenzyme Q10 (CoQ10) supplementation on myocardial apoptotic proteins in obese male rats. Forty-eight male Wistar rats were randomly assigned to 6 groups including non-obese control (NOC), baseline obese control (BOC), HIIT, CoQ10, HIIT + CoQ10, and control. NOC and BOC groups were sacrificed at the beginning of the study. Exercise groups were subjected to a HIIT program over 12 weeks. Rats in CoQ10 group were gavage-fed with 500 mg/kg-1 CoQ10 supplement throughout the study. The heart muscle was removed 48 hours after the last training session. The B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), cytochrome c, BH3-interacting domain death agonist (Bid), caspase-8, and caspase-3 protein expressions were analyzed using western blotting. Data were analyzed using independent t-test and two-way analysis of variance (ANOVA). The Bax, Bid, cytochrome c, caspase-8, caspase-3 proteins, and Bax/Bcl-2 were significantly higher in BOC group compared to NOC (P = 0.025, P = 0.0001, P = 0.013, P = 0.017, P = 0.010, P = 0.180, respectively). Moreover, Bcl-2 protein was lower in BOC compared to NOC group (P = 0.025). HIIT program decreased Bax/Bcl-2 ratio (P = 0.012), Bid (P = 0.0001), cytochrome c (P = 0.003), caspase-8 (P = 0.006), and caspase-3 (P = 0.002) proteins and increased Bcl-2 (P = 0.001) proteins in heart muscle. CoQ10 supplementation significantly increased Bcl-2 protein content (P = 0.001). HIIT exerts an anti-apoptotic effect in heart muscle of obese rats. Although the administration of CoQ10 increased Bcl-2 anti-apoptotic protein, it did not show a potent synergistic effect along with HIIT to reduce obesity-related myocardial apoptosis.

Antioxidant and anti-inflammatory properties of gamma- oryzanol attenuates insulin resistance by increasing GLUT- 4 expression in skeletal muscle of obese animals

BackgroundSkeletal muscle is the most important organ for whole-body glucose homeostasis. However, it has been suggested that obesity-related inflammation could be involved in insulin resistance and diabetes mellitus type 2 (DM2) development due several mechanisms, among them, the reduced expression of the glucose transporter type 4 (GLUT-4). Gamma-oryzanol (γOz) is a compound present in the whole grain of rice that presents anti-inflammatory and antioxidant activities. The aim of this study was to verify if the effect antioxidant and anti-inflammatory of yOz attenuate insulin resistance in skeletal muscle of obese rats by increasing GLUT- 4 expression. MethodsMale Wistar rats (±187 g) were initially randomly distributed into 2 experimental groups (control, n = 6, and high sugar-fat diet (HSF), n = 12) for 20 weeks. At week 20th of this study, once obesity and insulin resistance were detected in the HSF group, animals were divided to begin the treatment with γOz or continue receiving HSF for 10 more weeks. At the end it was analyzed nutritional, metabolic, inflammatory and oxidative stress parameters and GLUT-4 protein expression. ResultsThe treatment improved insulin resistance, reduced inflammation, increased antioxidant response and GLUT-4 expression. ConclusionIt is possible to conclude that the antioxidant and anti-inflammatory activity of yOz attenuates insulin resistance by increasing GLUT-4 expression in skeletal muscle of obese animals.

Inhibition of miR-27b Regulates Lipid Metabolism in Skeletal Muscle of Obese Rats During Hypoxic Exercise by Increasing PPARγ Expression.

Hypoxic exercise may represent a novel therapeutic strategy to reduce and prevent obesity through the regulation of lipid metabolism. During hypoxic exercise, the targeting of peroxisome proliferator-activated receptor gamma (PPARγ) by miR-27b has been proposed to be one of the mechanisms involved in the modulation of lipid metabolism. We have previously shown that miR-27b can repress PPARγ and lipid metabolism-associated factors, thereby affecting lipid metabolism during hypoxic exercise in a rat model of obesity. In the current study, we aimed to confirm the role of miR-27b in the regulation of lipid metabolism. First, miR-27b expression was either upregulated or downregulated through the injection of adeno-associated virus (AAV) 9 containing a miR-27b expression cassette or miR-27b-3p inhibitor, respectively, into the right gastrocnemius muscle of obese rats. The rats were then subjected to a 4-week program of hypoxic exercise, and a series of parameters related to lipid metabolism were systematically evaluated, including body composition, blood lipid levels, miR-27b RNA levels, and mRNA and protein levels of PPARγ and those of its downstream lipid metabolism-associated factors. No significant differences were found in body composition between rats expressing different levels of miR-27b. However, regarding blood lipids, miR-27b overexpression led to increased concentrations of triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and free fatty acids (FFAs), while inhibition of miR-27b decreased the total cholesterol (TC) level and increased that of high-density lipoprotein cholesterol (HDL-C). At the mRNA level, miR-27b overexpression downregulated the expression of Pparγ, but upregulated that of lipid metabolism-associated factors such as heart-type fatty acid-binding protein (H-FABP), fatty acid transport protein 1 (FATP1), adipose triglyceride lipase (ATGL), and lipoprotein lipase (LPL), whereas miR-27b inhibition elicited the opposite effect; however, inhibition of miR-27b led to elevated cholesterol 7 alpha-hydroxylase (CYP7A1) and fatty acid translocase 36 (CD36) levels. Similarly, at the protein level, miR-27b overexpression promoted a decrease in the concentration of PPARγ, whereas miR-27b inhibition led to an increase in PPARγ levels, as well as those of CYP7A1, CD36, ATGL, and LPL. Overall, our results indicated that hypoxic exercise regulates lipid metabolism via the miR-27b/PPARγ pathway and modulates ATGL and LPL expression through inducing their post-transcriptional modifications.

A single session of physical activity restores the mitochondrial organization disrupted by obesity in skeletal muscle fibers

BackgroundSeveral studies have proved that physical activity (PA) regulates energetic metabolism associated with mitochondrial dynamics through AMPK activation in healthy subjects. Obesity, a condition that induces oxidative stress, mitochondrial dysfunction, and low AMPK activity leads to mitochondrial fragmentation. However, few studies describe the effect of PA on mitochondrial dynamics regulation in obesity. AimThe present study aimed to evaluate the effect of a single session of PA on mitochondrial dynamics regulation as well as its effect on mitochondrial function and organization in skeletal muscles of obese rats (Zucker fa/fa). Main methodsMale Zucker lean and Zucker fa/fa rats aged 12 to 13 weeks were divided into sedentary and subjected-to-PA (single session swimming) groups. Gastrocnemius muscle was dissected into isolated fibers, mitochondria, mRNA, and total proteins for their evaluation. Key findingsThe results showed that PA increased the Mfn-2 protein level in the lean and obese groups, whereas Drp1 levels decreased in the obese group. OMA1 protease levels increased in the lean group and decreased in the obese group. Additionally, AMPK analysis parameters (expression, protein level, and activity) did not increase in the obese group. These findings correlated with the partial restoration of mitochondrial function in the obese group, increasing the capacity to maintain the membrane potential after adding calcium as a stressor, and increasing the transversal organization level of the mitochondria analyzed in isolated fibers. SignificanceThese results support the notion that obese rats subjected to PA maintain mitochondrial function through mitochondrial fusion activation by an AMPK-independent mechanism.

Effects of Aerobic and Resistance Exercise on Myokines in High Fat Diet-Induced Middle-Aged Obese Rats.

The objective of this study was to analyze the effects of aerobic and resistance exercise on myokines expression in the skeletal muscle of middle-aged rats with high fat diet-induced obesity, to investigate the feasibility of using exercise training to reduce inflammation. Male 50-week-old Sprague Dawley rats were divided into normal diet, normal diet + exercise, high fat diet, and high fat diet + exercise groups. After six weeks on a high fat diet to induce obesity, a 12-week exercise program was implemented, which combined aerobic exercise (treadmill running) and resistance exercise (ladder climbing) three times a week for 75 min per session. We analyzed the protein levels of interleukins (IL) 6, 7, and 8, C-X-C motif chemokine receptor 2, and vascular endothelial growth factor in skeletal muscles by western blotting. Body weight decreased significantly during the 12-week exercise program in the exercise groups compared to the non-exercise groups (p < 0.05). The levels of all myokines analyzed were significantly lower in the skeletal muscle of the high fat diet group compared to the normal diet group (p < 0.05). After completing the 12-week exercise program, IL-7, IL-8, C-X-C motif chemokine receptor 2, and vascular endothelial growth factor expressions were significantly higher in the high fat diet + exercise group compared to the high fat diet group (p < 0.05). However, while IL-6 expression was significantly lower in the high fat diet and high fat diet + exercise groups compared to the normal diet group (p < 0.05), it was not significantly affected by exercise. In conclusion, high fat diet-induced obesity resulted in decreased myokines in the skeletal muscles, but combined exercise training of aerobic and resistance exercise increased myokines secretion in the skeletal muscle of obese rats, and is thought to help reduce inflammation.

The Oxidative Stress Markers in the Erythrocytes and Heart Muscle of Obese Rats: Relate to a High-Fat Diet but Not to DJOS Bariatric Surgery.

Obesity and high-fat diet (HF) are prevalent causes of oxidative stress (OS). Duodenal-jejunal omega switch (DJOS) is a bariatric procedure used for body mass reduction, extensively tested in animal models. We studied the long-term impact of bariatric surgery and an HF diet on the oxidative stress markers in erythrocytes and heart muscles of rats. We analyzed superoxide dismutase (SOD), catalase (CAT), glutathione transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx) activity and malondialdehyde (MDA) concentration in DJOS or SHAM (control) operated rats fed with different dietary protocols (control diet (CD) and high-fat diet (HF)), before and after the surgery (CD/CD, HF/HF, CD/HF, and HF/CD). We observed higher erythrocytes CAT, GST and GPx activity in DJOS-operated (vs. SHAM) rats fed with an HF/HF diet. For DJOS-operated rats, erythrocytes CAT and GPx activity and MDA concentration were significantly lower in CD/CD group. We observed increased heart muscle GR activity in SHAM-operated rats (vs. DJOS bariatric surgery) fed with an HF/HF diet. Change from HF to CD diet increased heart muscle GPx activity after DJOS bariatric surgery. Heart muscle SOD activity was lower in HF/HF and CD/CD groups after DJOS bariatric surgery (vs. SHAM). DJOS surgery significantly reduced heart muscle MDA concentration in HF/HF and HF/CD groups (vs. SHAM). We conclude that the selected dietary patterns had a stronger impact on oxidative stress markers in erythrocytes and heart muscle than DJOS bariatric surgery.

Carbenoxolone enhances peripheral insulin sensitivity and GLUT4 expression in skeletal muscle of obese rats: Potential participation of UBC9 protein

AimThis study investigates the insulin sensitizer effect of carbenoxolone (CBX) and potentially involved peripheral mechanisms. Main methodsTaking glucose transporter 4 (GLUT4) as a marker of glucose disposal, we investigated the CBX effects on whole-body insulin sensitivity and solute carrier 2a4 (Slc2a4)/GLUT4 expression in visceral (VAT) and subcutaneous (SAT) adipose tissues and soleus muscle of monosodium glutamate (MSG)-induced obese rats. Sterol regulatory element binding protein (SREBP1), an enhancer of Slc2a4 expression was analyzed through mRNA content and SREBP1-binding to Slc2a4 promoter. Finally, the small ubiquitin-modifier conjugating enzyme 9 (UBC9), whose low content indicates accelerated GLUT4 degradation was analyzed in soleus. Key findingsHypercorticosteronemia, hyperinsulinemia and low glucose decay rate in the insulin tolerance test of obese rats were restored by CBX (P < 0.05). Slc2a4/GLUT4 increased in SAT (P < 0.05) and decreased in VAT (P < 0.01) of obese rats. In soleus, obesity increased Slc2a4 but decreased GLUT4 (P < 0.01), possibly by accelerating GLUT4 degradation, as suggested by decreased UBC9 (P < 0.01). CBX restored both UBC9 and GLUT4 contents. SREBP1 did not participate in the Slc2a4 transcriptional regulation. SignificanceThe insulin sensitizer effect of CBX involves the increase of GLUT4 expression in soleus, indicating an increased glucose disposal in skeletal muscle. This observation reinforces the skeletal muscle as the main site of insulin-induced glucose uptake and sheds new light on the metabolic effects of 11βHSD1 inhibitors, since most of the studies so far have focused on its effects on liver and adipose tissues.

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

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.&#x0D; 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.&#x0D; 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 &lt; 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 &lt; 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 &lt; 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 &lt; 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 &lt; 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 &lt; 0. 05).&#x0D; 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.

Histological observation of leptin receptor in skeletal muscle in obese rats with periodontitis

Histological observation of leptin receptor in skeletal muscle in obese rats with periodontitis

High, but not low, exercise volume shifts the balance of renin-angiotensin system toward ACE2/Mas receptor axis in skeletal muscle in obese rats.

Metabolic syndrome is a cluster of metabolic risk factors that is linked to central obesity, elevated blood pressure, insulin resistance (IR), and dyslipidemia, where the renin-angiotensin system (RAS) may provide a link among them. This study aimed to evaluate volume exercise effects comparing low vs. high volume of chronic aerobic exercise on RAS axes in skeletal muscle in a diet-induced obesity (DIO) rat model. For this, male Wistar-Kyoto rats were fed a standard chow (SC) diet or a high-fat (HF) diet for 32 wk. Animals receiving the HF diet were randomly divided into low exercise volume (LEV, 150 min/wk) and high exercise volume (HEV, 300 min/wk) at the 20th week. After 12 wk of aerobic treadmill training, the body mass and composition, blood pressure, glucose and lipid metabolism, RAS axes, insulin signaling, and inflammatory pathway were performed. HEV slowed the body mass gain, reduced intra-abdominal fat pad and leptin levels, improved total and peripheral body composition and inflammatory cytokine, reduced angiotensin II type 1 receptor expression, and increased Mas receptor protein expression compared with the HF animals. Sedentary groups (SC and HF) presented lower time to exhaustion and maximal velocity compared with the LEV and HEV groups. Both exercise training groups showed reduced resting systolic blood pressure and heart rate, improved glucose tolerance, IR, insulin signaling, and lipid profile. We conclude that the HEV, but not LEV, shifted the balance of RAS toward the ACE2/Mas receptor axis in skeletal muscle, presenting protective effects against the DIO model.

Obesity-induced discrepancy between contractile and metabolic phenotypes in slow- and fast-twitch skeletal muscles of female obese Zucker rats.

A clear picture of skeletal muscle adaptations to obesity and related comorbidities remains elusive. This study describes fiber-type characteristics (size, proportions, and oxidative enzyme activity) in two typical hindlimb muscles with opposite structure and function in an animal model of genetic obesity. Lesser fiber diameter, fiber-type composition, and histochemical succinic dehydrogenase activity (an oxidative marker) of muscle fiber types were assessed in slow (soleus)- and fast (tibialis cranialis)-twitch muscles of obese Zucker rats and compared with age (16 wk)- and sex (females)-matched lean Zucker rats (n = 16/group). Muscle mass and lesser fiber diameter were lower in both muscle types of obese compared with lean animals even though body weights were increased in the obese cohort. A faster fiber-type phenotype also occurred in slow- and fast-twitch muscles of obese rats compared with lean rats. These adaptations were accompanied by a significant increment in histochemical succinic dehydrogenase activity of slow-twitch fibers in the soleus muscle and fast-twitch fiber types in the tibialis cranialis muscle. Obesity significantly increased plasma levels of proinflammatory cytokines but did not significantly affect protein levels of peroxisome proliferator-activated receptors PPARγ or PGC1α in either muscle. These data demonstrate that, in female Zucker rats, obesity induces a reduction of muscle mass in which skeletal muscles show a diminished fiber size and a faster and more oxidative phenotype. It was noteworthy that this discrepancy in muscle's contractile and metabolic features was of comparable nature and extent in muscles with different fiber-type composition and antagonist functions.NEW & NOTEWORTHY This study demonstrates a discrepancy between morphological (reduced muscle mass), contractile (shift toward a faster phenotype), and metabolic (increased mitochondrial oxidative enzyme activity) characteristics in skeletal muscles of female Zucker fatty rats. It is noteworthy that this inconsistency was comparable (in nature and extent) in muscles with different structure and function.

Mangiferin protects against adverse skeletal muscle changes and enhances muscle oxidative capacity in obese rats.

Obesity-related skeletal muscle changes include muscle atrophy, slow-to-fast fiber-type transformation, and impaired mitochondrial oxidative capacity. These changes relate with increased risk of insulin resistance. Mangiferin, the major component of the plant Mangifera indica, is a well-known anti-inflammatory, anti-diabetic, and antihyperlipidemic agent. This study tested the hypothesis that mangiferin treatment counteracts obesity-induced fiber atrophy and slow-to-fast fiber transition, and favors an oxidative phenotype in skeletal muscle of obese rats. Obese Zucker rats were fed gelatin pellets with (15 mg/kg BW/day) or without (placebo group) mangiferin for 8 weeks. Lean Zucker rats received the same gelatin pellets without mangiferin and served as non-obese and non-diabetic controls. Lesser diameter, fiber composition, and histochemical succinic dehydrogenase activity (an oxidative marker) of myosin-based fiber-types were assessed in soleus and tibialis cranialis muscles. A multivariate discriminant analysis encompassing all fiber-type features indicated that obese rats treated with mangiferin displayed skeletal muscle phenotypes significantly different compared with both lean and obese control rats. Mangiferin significantly decreased inflammatory cytokines, preserved skeletal muscle mass, fiber cross-sectional size, and fiber-type composition, and enhanced muscle fiber oxidative capacity. These data demonstrate that mangiferin attenuated adverse skeletal muscle changes in obese rats.