scholarly journals Type 2 diabetes causes skeletal muscle atrophy but does not impair resistance training‐mediated myonuclear accretion and muscle mass gain in rats

2019 ◽  
Vol 104 (10) ◽  
pp. 1518-1531 ◽  
Author(s):  
Satoru Ato ◽  
Kohei Kido ◽  
Koji Sato ◽  
Satoshi Fujita
2020 ◽  
Vol 8 (1) ◽  
pp. e001027 ◽  
Author(s):  
Tomonori Kimura ◽  
Takuro Okamura ◽  
Keiko Iwai ◽  
Yoshitaka Hashimoto ◽  
Takafumi Senmaru ◽  
...  

ObjectiveReduction of muscle mass and strength is an important treatment target for patients with type 2 diabetes. Recent studies have reported that high-intensity resistance training improves physical function; however, all patients found it difficult to perform high-intensity resistance training. Radio calisthenics, considered as therapeutic exercises to promote health in Japan, are simple exercises that can be performed regardless of age and help move the muscles and joints of the whole body effectively according to the rhythm of radio. We investigated the efficacy of radio calisthenics for muscle mass in patients with type 2 diabetes in this retrospective cohort study.Research design and methodsA total of 42 hospitalized patients with type 2 diabetes were recruited. The skeletal muscle mass index (SMI, kg/m2) was calculated as appendicular muscle mass (kg) divided by height squared (m2). We defined the change of SMI as the difference of SMI between the beginning and end of hospitalization.ResultsAmong 42 patients, 15 (11 men and 4 women) performed radio calisthenics. Body weights of both radio calisthenics exercisers and non-exercisers decreased during hospitalization. The change of SMI was significantly lesser in radio calisthenics exercisers than in non-exercisers (7.1±1.4 to 7.1±1.3, –0.01±0.09 vs 6.8±1.1 to 6.5±1.2, –0.27±0.06 kg/m2, p=0.016). The proportion of decreased SMI was 85.2% (23/27 patients) in non-radio calisthenics exercisers, whereas that in radio calisthenics exercisers was 46.7% (7/15 patients).ConclusionsRadio calisthenics prevent the reduction of skeletal muscle mass. Thus, radio calisthenics can be considered effective for patients with type 2 diabetes.


Diabetologia ◽  
2021 ◽  
Author(s):  
Shu Yang ◽  
Guangyan Yang ◽  
Han Wu ◽  
Lin Kang ◽  
Jiaqing Xiang ◽  
...  

Abstract Aims/hypothesis Type 2 diabetes is associated with a reduction in skeletal muscle mass; however, how the progression of sarcopenia is induced and regulated remains largely unknown. We aimed to find out whether a specific microRNA (miR) may contribute to skeletal muscle atrophy in type 2 diabetes. Methods Adeno-associated virus (AAV)-mediated skeletal muscle miR-193b overexpression in C57BLKS/J mice, and skeletal muscle miR-193b deficiency in db/db mice were used to explore the function of miR-193b in muscle loss. In C57BL/6 J mice, tibialis anterior-specific deletion of 3-phosphoinositide-dependent protein kinase-1 (PDK1), mediated by in situ AAV injection, was used to confirm whether miR-193b regulates muscle growth through PDK1. Serum miR-193b levels were also analysed in healthy individuals (n = 20) and those with type 2 diabetes (n = 20), and correlations of miR-193b levels with HbA1c, fasting blood glucose (FBG), body composition, triacylglycerols and C-peptide were assessed. Results In this study, we found that serum miR-193b levels increased in individuals with type 2 diabetes and negatively correlated with muscle mass in these participants. Functional studies further showed that AAV-mediated overexpression of miR-193b induced muscle loss and dysfunction in healthy mice. In contrast, suppression of miR-193b attenuated muscle loss and dysfunction in db/db mice. Mechanistic analysis revealed that miR-193b could target Pdk1 expression to inactivate the Akt/mammalian target of rapamycin (mTOR)/p70S6 kinase (S6K) pathway, thereby inhibiting protein synthesis. Therefore, knockdown of PDK1 in healthy mice blocked miR-193b-induced inactivation of the Akt/mTOR/S6K pathway and impairment of muscle growth. Conclusions/interpretation Our results identified a previously unrecognised role of miR-193b in muscle function and mass that could be a potential therapeutic target for treating sarcopenia. Graphical abstract


2020 ◽  
Author(s):  
Jürgen G. Okun ◽  
Patricia M. Rusu ◽  
Andrea Y. Chan ◽  
Yann W. Yap ◽  
Thomas Sharkie ◽  
...  

AbstractBoth obesity and sarcopenia are frequently associated in ageing, and together may promote the progression of related conditions such as diabetes and frailty. However, little is known about the pathophysiological mechanisms underpinning this association. Here we uncover dysregulated systemic alanine metabolism and hyper-expression of the alanine transaminases (ALT) in the liver of obese/diabetic mice and humans. Hepatocyte-selective silencing of both ALT enzymes revealed a clear role in systemic alanine clearance which related to glycemic control. In obese/diabetic mice, not only did silencing both ALT enzymes retard hyperglycemia, but also reversed skeletal muscle atrophy. This was due to a rescue of depressed skeletal muscle protein synthesis, with a liver-skeletal muscle amino acid metabolic crosstalk exemplified by ex vivo experiments. Mechanistically, chronic liver glucocorticoid and glucagon signaling driven liver alanine catabolism promoted hyperglycemia and skeletal muscle wasting. Taken together, here we reveal an endocrine-hepato-muscular metabolic cycle linking hyperglycemia and skeletal muscle atrophy in type 2 diabetes.


Life Sciences ◽  
2020 ◽  
Vol 258 ◽  
pp. 118243 ◽  
Author(s):  
Zhen Fan ◽  
Jing Wu ◽  
Qiu-nan Chen ◽  
An-kang Lyu ◽  
Jin-liang Chen ◽  
...  

2021 ◽  
Vol 3 (3) ◽  
pp. 394-409
Author(s):  
Jürgen G. Okun ◽  
Patricia M. Rusu ◽  
Andrea Y. Chan ◽  
Yuqin Wu ◽  
Yann W. Yap ◽  
...  

2018 ◽  
Author(s):  
Se-Hwa Kim ◽  
Soo-Kyung Kim ◽  
Young-Ju Choi ◽  
Seok-Won Park ◽  
Eun-Jig Lee ◽  
...  

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 771-P
Author(s):  
SODAI KUBOTA ◽  
HITOSHI KUWATA ◽  
SAKI OKAMOTO ◽  
DAISUKE YABE ◽  
KENTA MUROTANI ◽  
...  

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Akira Nemoto ◽  
Toru Goyagi

Abstract Background Sarcopenia promotes skeletal muscle atrophy and exhibits a high mortality rate. Its elucidation is of the highest clinical importance, but an animal experimental model remains controversial. In this study, we investigated a simple method for studying sarcopenia in rats. Results Muscle atrophy was investigated in 24-week-old, male, tail-suspended (TS), Sprague Dawley and spontaneously hypertensive rats (SHR). Age-matched SD rats were used as a control group. The skeletal muscle mass weight, muscle contraction, whole body tension (WBT), cross-sectional area (CSA), and Muscle RING finger-1 (MuRF-1) were assessed. Enzyme-linked immunosorbent assay was used to evaluate the MuRF-1 levels. Two muscles, the extensor digitorum longus and soleus muscles, were selected for representing fast and slow muscles, respectively. All data, except CSA, were analyzed by a one-way analysis of variance, whereas CSA was analyzed using the Kruskal-Wallis test. Muscle mass weight, muscle contraction, WBT, and CSA were significantly lower in the SHR (n = 7) and TS (n = 7) groups than in the control group, whereas MuRF-1 expression was dominant. Conclusions TS and SHR presented sarcopenic phenotypes in terms of muscle mass, muscle contraction and CSA. TS is a useful technique for providing muscle mass atrophy and weakness in an experimental model of sarcopenia in rats.


Diabetes Care ◽  
2017 ◽  
Vol 40 (9) ◽  
pp. 1256-1263 ◽  
Author(s):  
Ryan D. Russell ◽  
Donghua Hu ◽  
Timothy Greenaway ◽  
Sarah J. Blackwood ◽  
Renee M. Dwyer ◽  
...  

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