scholarly journals Resveratrol attenuates high-fat diet-induced obesity and the aging-related sarcopenia mitochondrial dysfunction in skeletal muscle

2019 ◽  
Author(s):  
Chyi-Huey Bai ◽  
Javad Alizargar ◽  
Jia-Ping Wu

AbstractSarcopenic obesity is a progressive loss of skeletal muscle mass and strength with increases in adiposity. The aim of this study was to investigate the effects of resveratrol on obesity or sarcopenia to potential therapy risk for skeletal muscle declines in physical function. C57BL/6J male mice were fed either a high-fat diet for 4 weeks and resveratrol (low-, middle-, and high-dose) for 8 weeks to express the obesity effect. Samp8 mice sarcopenia skeletal muscle functional deterioration expressed an age-associated decline. Resveratrol (150 mg/Kg BW, daily) was administered by oral gavage two times a week one month of the experimental period. Exercise training based on adaptations in the muscle is training twice a week for 4 weeks. The skeletal muscles from mice in each group were analyzed by H&E staining, TUNEL and western blot analysis to determine mitochondrial function expression, apoptosis and relative fibrosis signaling. Results of the present study indicate that resveratrol in obesity skeletal muscle is linked to an increase in the expression of mitochondrial function involved in Bcl-2 and PI3K/AKT. On the other hand, resveratrol attenuates sarcopenia Samp8 mice, the age-related loss of skeletal muscle mass and mitochondrial function involved in Bad, caspase 3 and IL-6/ERK1. However, exercise training not find a significant difference in sarcopenia skeletal muscles SAMP8 mice. Exercise training didn’t induce sarcopenia skeletal muscle hypertrophy in sarcopenic SAMP8 mice. Therefore, we suggest that resveratrol as a therapeutic potential in the combination of sarcopenia and obesity, the state called sarcopenic obesity.

2021 ◽  
Author(s):  
Aliyu Tijani Jibril ◽  
Atieh Mirzababaei ◽  
Farideh Shiraseb ◽  
Niloufar Rasaei ◽  
Khadijeh Mirzaei

Abstract Objectives Obesity is a major risk factor for metabolic syndrome, with its prevalence has increased over the past decade. Major changes in body composition with aging have a significant effect on many clinical outcomes. Sarcopenic obesity consists of both the presence of abnormal adipose tissue with a deficit of muscle mass. Results Of the 241 subjects in this study (average age 35.32 years), 176 (73.03%) were classified as MUO phenotype. Based on this study, the prevalence of sarcopenic obesity was 7.88%. We found that high fat-free mass was more strongly and significantly associated with MUO phenotype. Furthermore, we found that individuals with high fat-free mass and high skeletal muscle mass had a significantly low prevalence of MUO phenotype. A significant positive correlation between metabolic phenotypes and sarcopenic obesity was also observed after all potential covariates were adjusted for. These results of this study suggest that increased adiposity and decreased skeletal muscle mass are associated with unfavorable metabolic traits among overweight and obese Iranian women. SO was also found to be associated with a greater risk of developing MUO phenotype.


Author(s):  
Jun-Won Heo ◽  
Su-Zi Yoo ◽  
Mi-Hyun No ◽  
Dong-Ho Park ◽  
Ju-Hee Kang ◽  
...  

Obesity is characterized by the induction of skeletal muscle remodeling and mitochondria-mediated apoptosis. Exercise has been reported as a positive regulator of skeletal muscle remodeling and apoptosis. However, the effects of exercise on skeletal muscle remodeling and mitochondria-mediated apoptosis in obese skeletal muscles have not been clearly elucidated. Four-week-old C57BL/6 mice were randomly assigned into four groups: control (CON), control plus exercise (CON + EX), high-fat diet (HFD), and HFD plus exercise groups (HFD + EX). After obesity was induced by 20 weeks of 60% HFD feeding, treadmill exercise was performed for 12 weeks. Exercise ameliorated the obesity-induced increase in extramyocyte space and a decrease in the cross-sectional area of the skeletal muscle. In addition, it protected against increases in mitochondria-mediated apoptosis in obese skeletal muscles. These results suggest that exercise as a protective intervention plays an important role in regulating skeletal muscle structure and apoptosis in obese skeletal muscles.


2011 ◽  
Vol 300 (3) ◽  
pp. E543-E553 ◽  
Author(s):  
Masashi Nakatani ◽  
Masahiro Kokubo ◽  
Yutaka Ohsawa ◽  
Yoshihide Sunada ◽  
Kunihiro Tsuchida

Myostatin, a member of the transforming growth factor (TGF)-β superfamily, plays a potent inhibitory role in regulating skeletal muscle mass. Inhibition of myostatin by gene disruption, transgenic (Tg) expression of myostatin propeptide, or injection of propeptide or myostatin antibodies causes a widespread increase in skeletal muscle mass. Several peptides, in addition to myostatin propeptide and myostatin antibodies, can bind directly to and neutralize the activity of myostatin. These include follistatin and follistatin-related gene. Overexpression of follistatin or follistatin-related gene in mice increased the muscle mass as in myostatin knockout mice. Follistatin binds to myostatin but also binds to and inhibits other members of the TGF-β superfamily, notably activins. Therefore, follistatin regulates both myostatin and activins in vivo. We previously reported the development and characterization of several follistatin-derived peptides, including FS I-I (Nakatani M, Takehara Y, Sugino H, Matsumoto M, Hashimoto O, Hasegawa Y, Murakami T, Uezumi A, Takeda S, Noji S, Sunada Y, Tsuchida K. FASEB J 22: 477–487, 2008). FS I-I retained myostatin-inhibitory activity without affecting the bioactivity of activins. Here, we found that inhibition of myostatin increases skeletal muscle mass and decreases fat accumulation in FS I-I Tg mice. FS I-I Tg mice also showed decreased fat accumulation even on a control diet. Interestingly, the adipocytes in FS I-I Tg mice were much smaller than those of wild-type mice. Furthermore, FS I-I Tg mice were resistant to high-fat diet-induced obesity and hepatic steatosis and had lower hepatic fatty acid levels and altered fatty acid composition compared with control mice. FS I-I Tg mice have improved glucose tolerance when placed on a high-fat diet. These data indicate that inhibiting myostatin with a follistatin-derived peptide provides a novel therapeutic option to decrease adipocyte size, prevent obesity and hepatic steatosis, and improve glucose tolerance.


2020 ◽  
Author(s):  
Aliyu Tijani Jibril ◽  
Atieh Mirzababaei ◽  
Farideh Shiraseb ◽  
Niloufar Rasaei ◽  
Khadijeh - Mirzaei

Abstract Background Obesity is a major risk factor for metabolic syndrome, with its prevalence has increased over the past decade. Major changes in body composition with aging have a significant effect on many clinical outcomes. Sarcopenic obesity consists of both the presence of abnormal adipose tissue with a deficit of muscle mass. Methods This cross-sectional study was conducted among a total of 241 overweight/obese women aged between 18–48 years in Tehran, Iran, registered by the use of the multistage cluster random sampling method. Blood samples were taken following standard procedures. Body composition was assessed through a multi-frequency bioelectrical impedance analyzer. The metabolic risk was assessed according to Karelis criteria and the subjects were classified as either MHO or MUO phenotypes. Results Of the 241 subjects in this study (average age 35.32 years), 176 (73.03%) were classified as MUO phenotype. Based on this study, the prevalence of sarcopenic obesity was 7.88%. We found that high fat-free mass was more strongly and significantly associated with MUO phenotype. Furthermore, we found that individuals with high fat-free mass and high skeletal muscle mass had a significantly low prevalence of MUO phenotype. A significant positive correlation between metabolic phenotypes and sarcopenic obesity was also observed after all potential covariates were adjusted for. Conclusion These results of this study suggest that increased adiposity and decreased skeletal muscle mass are associated with unfavorable metabolic traits among overweight and obese Iranian women. SO was also found to be associated with a greater risk of developing MUO phenotype.


Author(s):  
Katsuyuki Tokinoya ◽  
Seiko Ono ◽  
Kai Aoki ◽  
Koki Yanazawa ◽  
Yasuhiro Shishikura ◽  
...  

AbstractIntroductionExercise training is beneficial for reducing obesity. In particular, exercise training can lower the catecholamine concentration in circulation. Renalase, whose expression was first confirmed in the kidneys, is a physiologically active substance that decomposes circulating catecholamines; additionally, it has been reported to be present in the skeletal muscles. The aim of this study was to clarify the expression of renalase in the skeletal muscles and kidneys after high-intensity exercise training in obese mice.Material and methodsThe mice were divided into four groups: normal diet and sedentary, normal diet and exercise training, high-fat diet and sedentary, and high-fat diet and exercise training, and the test was performed for 8 weeks.ResultsBody weight and skeletal muscle wet weight were reduced by high-fat diet intake but were rescued by training. Skeletal muscle renalase gene expression was significantly increased by exercise training. However, in the kidneys the gene expression of renalase was significantly increased by high-fat diet intake and exercise training. No significant changes were observed in the gene expression of catecholamine-degrading enzymes, catechol-O-methyltransferase and monoamine oxidase A and B.ConclusionWe demonstrated that exercise training increased the gene expression of renalase in the skeletal muscles and kidneys, thus lowering circulating catecholamine levels. This may lead to amelioration of obesity as catecholamines are lipolytic.


2016 ◽  
Vol 24 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Weixiu Ji ◽  
Lijing Gong ◽  
Jianxiong Wang ◽  
Hui He ◽  
Ying Zhang

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anandini Swaminathan ◽  
Andrej Fokin ◽  
Tomas Venckūnas ◽  
Hans Degens

AbstractMethionine restriction (MR) has been shown to reduce the age-induced inflammation. We examined the effect of MR (0.17% methionine, 10% kCal fat) and MR + high fat diet (HFD) (0.17% methionine, 45% kCal fat) on body mass, food intake, glucose tolerance, resting energy expenditure, hind limb muscle mass, denervation-induced atrophy and overload-induced hypertrophy in young and old mice. In old mice, MR and MR + HFD induced a decrease in body mass. Muscle mass per body mass was lower in old compared to young mice. MR restored some of the HFD-induced reduction in muscle oxidative capacity. The denervation-induced atrophy of the m. gastrocnemius was larger in animals on MR than on a control diet, irrespective of age. Old mice on MR had larger hypertrophy of m. plantaris. Irrespective of age, MR and MR + HFD had better glucose tolerance compared to the other groups. Young and old mice on MR + HFD had a higher resting VO2 per body mass than HFD group. Mice on MR and MR + HFD had a resting respiratory quotient closer to 0.70, irrespective of age, indicating an increased utilization of lipids. In conclusion, MR in combination with resistance training may improve skeletal muscle and metabolic health in old age even in the face of obesity.


2015 ◽  
Vol 7 (3) ◽  
pp. 312-321 ◽  
Author(s):  
Stefanos Tyrovolas ◽  
Ai Koyanagi ◽  
Beatriz Olaya ◽  
Jose Luis Ayuso-Mateos ◽  
Marta Miret ◽  
...  

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