Muscle & nerve · 2016
Skeletal muscle dysfunction in the db/db mouse model of type 2 diabetes.
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Bayley Jeppe Seamus, Pedersen Thomas Holm, Nielsen Ole Baekgaard
Аннотация
INTRODUCTION: In this study we examined the mechanisms of motor dysfunction in type 2 diabetes.
METHODS: Contractile force was measured in isolated nerve-muscle preparations of db/db mice using various protocols for electrical stimulation. Sarcoplasmic reticulum Ca(2+) adenosine triphosphatase protein (SERCA) was quantified by comparing Ca(2+) -dependent and non-specific phosphorylation.
RESULTS: Compared 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.
CONCLUSIONS: The 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 Nerve 54: 460-468, 2016.
METHODS: Contractile force was measured in isolated nerve-muscle preparations of db/db mice using various protocols for electrical stimulation. Sarcoplasmic reticulum Ca(2+) adenosine triphosphatase protein (SERCA) was quantified by comparing Ca(2+) -dependent and non-specific phosphorylation.
RESULTS: Compared 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.
CONCLUSIONS: The 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 Nerve 54: 460-468, 2016.
Предметные рубрики MeSH
Adenosine TriphosphateAnalysis of VarianceAnimalsBody WeightCalciumDiabetes Mellitus, Type 2Disease Models, AnimalDose-Response Relationship, DrugElectric StimulationMiceMice, Mutant StrainsMuscle ContractionMuscle, SkeletalMuscular DiseasesMutationNicotinic AntagonistsPhosphorus IsotopesReceptors, LeptinSarcoplasmic Reticulum Calcium-Transporting ATPasesTubocurarine