scholarly journals Gene expression level of renalase in the skeletal muscles is increased with high-intensity exercise training in mice on a high-fat diet

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.

2020 ◽  
Vol 318 (4) ◽  
pp. E492-E503
Author(s):  
Kenichi Tanaka ◽  
Hirokazu Takahashi ◽  
Sayaka Katagiri ◽  
Kazuyo Sasaki ◽  
Yujin Ohsugi ◽  
...  

Sodium-glucose cotransporter 2 inhibitors (SGLT2is) have been reported to improve obesity, diabetes, and nonalcoholic fatty liver disease (NAFLD) in addition to exercise training, whereas the combined effects remain to be elucidated fully. We investigated the effect of the combination of the SGLT2i canagliflozin (CAN) and exercise training in high-fat diet-induced obese mice. High-fat diet-fed mice were housed in normal cages (sedentary; Sed) or wheel cages (WCR) with or without CAN (0.03% of diet) for 4 wk. The effects on obesity, glucose metabolism, and hepatic steatosis were evaluated in four groups (Control/Sed, Control/WCR, CAN/Sed, and CAN/WCR). Numerically additive improvements were found in body weight, body fat mass, blood glucose, glucose intolerance, insulin resistance, and the fatty liver of the CAN/WCR group, whereas CAN increased food intake and reduced running distance. Exercise training alone, CAN alone, or both did not change the weight of skeletal muscle, but microarray analysis showed that each resulted in a characteristic change of gene expression in gastrocnemius muscle. In particular, in the CAN/WCR group, there was acceleration of the angiogenesis pathway and suppression of the adipogenesis pathway compared with the CAN/Sed group. In conclusion, the combination of an SGLT2i and exercise training improves obesity, insulin resistance, and NAFLD in an additive manner. Changes of gene expression in skeletal muscle may contribute, at least in part, to the improvement of obesity and insulin sensitivity.


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.


2007 ◽  
Vol 293 (3) ◽  
pp. H1553-H1563 ◽  
Author(s):  
Yan Yang ◽  
Allan W. Jones ◽  
Tom R. Thomas ◽  
Leona J. Rubin

Potassium channels in vascular smooth muscle (VSM) control vasodilation and are potential regulatory targets. This study evaluated effects of sex differences, exercise training (EX), and high-fat diet (HF) on K+ currents ( IK) of coronary VSM cells. Yucatan male and female swine were assigned to either sedentary confinement (SED), 16 wk of EX, 20 wk of HF, or 20 wk of HF with 16 wk of EX (HF-EX). VSM cells of normal-diet SED animals exhibited three components of IK: 4-aminopyridine-sensitive IK(KV), TEA-sensitive IK(BK), and 4-aminopyridine + TEA-insensitive IK. Females exhibited significantly higher basal IK than males in the same group. EX increased basal IK in males and females. HF reduced IK in males and females and nullified effects of EX. Endothelin-1 increased IK significantly in males but not in females. In the presence of endothelin-1, 1) IK(KV) was similar in SED males and females and EX increased IK(KV) to a greater extent in males than in females and 2) IK(BK) was greater in SED females than in males and EX increased IK(BK) to a greater extent in males, resulting in IK(BK) similar to EX females. Importantly, HF nullified effects of EX on IK(KV) and IK(BK). These data indicate that basal IK of SED female swine is inherently greater than that shown in SED males and that males require EX to achieve comparable levels of IK. Importantly, HF reduced IK in males and females and nullified effects of EX, suggesting HF abrogates beneficial effects of EX on coronary smooth muscle.


2016 ◽  
Vol 4 (9) ◽  
pp. e12788 ◽  
Author(s):  
Jakob G. Knudsen ◽  
Ella Joensen ◽  
Laerke Bertholdt ◽  
Henrik Jessen ◽  
Line van Hauen ◽  
...  

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.


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

2017 ◽  
Vol 162 (1) ◽  
pp. 309-317 ◽  
Author(s):  
Jakob G Knudsen ◽  
Lærke Bertholdt ◽  
Anders Gudiksen ◽  
Sabine Gerbal-Chaloin ◽  
Martin Krøyer Rasmussen

2016 ◽  
Vol 62 (Suppl.1) ◽  
pp. 144-145
Author(s):  
SAORI KAKEHI ◽  
YOSHIFUMI TAMURA ◽  
KAGEUMI TAKENO ◽  
YUKO SAKURAI ◽  
MINAKO KAWAGUCHI ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document