Skeletal muscle dysfunction in the db/db mouse model of type 2 diabetes
Skeletal muscle dysfunction in the db/db mouse model of type 2 diabetes
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DOI：
10.1002/mus.25064
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发表时间：
2016-09-01
期刊：
影响因子：
3.4
通讯作者：
Nielsen, Ole Baekgaard
中科院分区：
文献类型：
--
作者：
Bayley, Jeppe Seamus;Pedersen, Thomas Holm;Nielsen, Ole Baekgaard
在这项研究中，我们探讨了2型糖尿病运动功能障碍的机制。方法采用不同的电刺激方案，测量db/db小鼠离体神经-肌肉制剂的收缩力。通过比较Ca2+依赖性和非特异性磷酸化，定量测定肌浆网Ca2+腺苷三磷酸酶蛋白（SERCA）。结果与对照组相比，经神经刺激后，db/db小鼠肌肉-神经制剂出现肌肉萎缩、轴突兴奋性降低和力缺陷。收缩后肌肉松弛减慢，SERCA含量降低。相反，神经肌肉接点对管碱的敏感性和肌纤维兴奋性不受影响。结论大鼠db/db肌的力缺损是由运动神经轴突功能障碍引起的神经肌肉信号传递萎缩和失败引起的。在糖尿病肌肉中普遍观察到的松弛速度减慢，在很大程度上可以解释为SERCA泵含量的减少。中国生物医学工程学报（英文版），2016
IntroductionIn this study we examined the mechanisms of motor dysfunction in type 2 diabetes.MethodsContractile force was measured in isolated nerve-muscle preparations of db/db mice using various protocols for electrical stimulation. Sarcoplasmic reticulum Ca2+ adenosine triphosphatase protein (SERCA) was quantified by comparing Ca2+-dependent and non-specific phosphorylation.ResultsCompared with controls, the muscle-nerve preparations of db/db mice displayed muscle atrophy, reduced axonal excitability, and force deficit when stimulated via the nerve. Muscle relaxation after contraction was slowed, and SERCA content was reduced. In contrast, the sensitivity of the neuromuscular junction to tubocurarine and muscle fiber excitability were not affected.ConclusionsThe force deficit in db/db muscles was caused by atrophy and failure of neuromuscular signal transmission related to motor nerve axonal dysfunction. The slowed relaxation rate generally observed in diabetic muscles can, to a large extent, be explained by decreased SERCA pump content. Muscle Nerve54: 460-468, 2016