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1.
Medical Journal of Tabriz University of Medical Sciences and Health Services. 2016; 38 (2): 6-13
in Persian | IMEMR | ID: emr-185214

ABSTRACT

Background and Objectives: Muscular atrophy is one of the most common complications of diabetes. In such cases, protein degradation isincreased and protein synthesisis decreased. MuRF1 is an E3 ubiquitin ligase which has been identified as a mediator of skeletal muscle wasting in various skeletal muscle atrophy models, and its expression is upregulated in atrophy. Exercise training has been suggested as one of the treatment strategies for muscular atrophy. The aim of this study is to investigate the effects of 4 weeks of resistance training on MuRF1 gene expression in muscular atrophy in streptozotocin-diabetic wistar rats


Material and Methods: Thirty six male Wister rats [288 +/- 22 g] were randomly divided into four groups: nondiabetic control, non-diabetic trained, diabetic control and diabetic trained. The exercise groups were subjected to a resistance training program using a ladder [3 days/wk, for 4 wk]. MuRF1 mRNA level was measured in Flexor Hallucis Longus muscle using Real-Time PCR. The results were studied by statistical methods


Results: MuRF1 gene expression was increased in rats with diabetes [p=0.001]; resistance training diminished the skeletal muscle wasting in diabetic rats [p=0.002] by inhibiting MuRF1 gene expression


Conclusion: This study indicates that short term resistance training can overcome diabetes-induced atrophy in rats. Whether this kind of training might be a good way for countering atrophy in other diseases with similar catabolic situation to diabetes remains to be elucidated

2.
Tehran University Medical Journal [TUMJ]. 2013; 71 (1): 37-45
in Persian | IMEMR | ID: emr-148045

ABSTRACT

Alpha-actinins are located in the skeletal muscle Z-line and form actin-actin cross-links. It belongs to a highly conserved family of actin-binding proteins- the spectrin superfamily, which also contains the spectrins and dystrophin. Mammalian skeletal muscle has two isoforms: alpha-actinins-2 and alpha-actinins-3. However, the response of alpha-actinins to exercise training is little understood. This study examined the effects of 8 weeks of resistance training on muscle mass, ACTN3 [alpha-actinins-3] gene expression levels and fiber type composition in the flexor hallucis longus [FHL] muscle. Forty five female Sprague-Dawley rats [Initial body mass: 169.25 +/- 9 gr age: 3 month] were obtained and assigned to a control [C; n=18] or exercise training [T; n=22] and pilot [P; n=5] groups. The resistance training consisted of climbing a ladder carrying a load suspended from the tail and the weight increased progressively. Real-time PCR and Immunohistochemistry techniques were used to measure gene expression levels and myosin heavy chain [MyHC] composition, respectively. Following 8 weeks of training, we observed significant increase in absolute muscle mass in FHL [P=0.01]. Results showed that no significant difference was found in ACTN3 gene expression levels between training and control groups [P=0.852 respectively]. Also, Pearson coefficient didn't indicated any significant relationships in gene expression and Fiber type IIX in response to resistance training in FHL [r=0.12]. However, resistance training effects on sarcomeric proteins development, these results showed no effect of resistance training on alpha-actinins-3 levels. Although alpha-actinins-3 has an important function to produce and progress of force in sarcomere, but didn't changed significantly in response to resistance training

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