Low-intensity pulsed ultrasound prevents muscle atrophy induced by type 1 diabetes in rats.

Low-intensity pulsed ultrasound prevents muscle atrophy induced by type 1 diabetes in rats.
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低强度脉冲超声预防 1 型糖尿病引起的大鼠肌肉萎缩

DOI:
10.1186/s13395-017-0145-7
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发表时间:
2017-12-22
期刊:
影响因子:
4.9
通讯作者:
Ta D
Ta D
中科院分区:
医学2区
文献类型:
--
作者:
Tang L;Li N;Jian W;Kang Y;Yin B;Sun S;Guo J;Sun L;Ta D

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背景1型糖尿病(T1 DM)可导致严重的骨骼肌萎缩。低强度脉冲超声(LIPUS)是骨骼肌损伤的常用治疗方法,可有效加速肌肉生长速度。然而,据我们所知,是否LIPUS可以改善骨骼肌萎缩在1型糖尿病rates.MethodsThe大鼠随机分为四组:正常对照组(NC);假治疗糖尿病对照组(DC);糖尿病,胰岛素治疗组(DI)作为阳性对照;和糖尿病LIPUS治疗组(DL)。DL大鼠用LIPUS(1 MHz,30 mW/cm 2)治疗腓肠肌20 min/d.Results6周后,DC组大鼠出现严重的肌萎缩。然而,LIPUS显著改善了1型糖尿病引起的肌肉萎缩,如显著增强的肌肉横截面积、肌肉质量和力量所证明的。与DC组相比,LIPUS可显著激活Akt,上调mTOR的表达,下调MIPUS及其受体ActRIIB和FoxO 1的表达。结论LIPUS可改善1型糖尿病所致的骨骼肌萎缩,MIPUS/Akt/mTOR和FoxO 1信号通路可能参与了LIPUS改善1型糖尿病所致骨骼肌萎缩的作用。
BackgroundType 1 diabetes mellitus (T1DM) induces serious skeletal muscle atrophy. Low-intensity pulsed ultrasound (LIPUS) is a common treatment for skeletal muscle injury and is effective in accelerating the rate of muscle growth. However, to the best of our knowledge, whether LIPUS can improve skeletal muscle atrophy in type 1 diabetic rats has not been investigated.MethodsThe rats were randomly divided into four groups: the normal control group (NC); the sham-treated diabetic control group (DC); the diabetic, insulin-treated group (DI) as a positive control; and the diabetic LIPUS therapy group (DL). The DL rats were treated with LIPUS (1 MHz, 30 mW/cm2) on the gastrocnemius for 20 min/day.ResultsAfter 6 weeks, the rats in the DC group showed severe muscle atrophy. However, LIPUS significantly improved type 1 diabetes-induced muscle atrophy, as evidenced by significantly enhanced muscle cross-sectional area, muscle mass, and strength. Moreover, compared with the DC group, LIPUS significantly activated Akt and upregulated the expression of mTOR, and LIPUS downregulated the expression of MSTN, its receptor ActRIIB, and FoxO1.ConclusionsThese results indicate that LIPUS improved muscle atrophy induced by type 1 diabetes, and the MSTN/Akt/mTOR&FoxO1 signaling pathway may play a role in this improvement.
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