title: Skeletal muscle dysfunction in the db/db mouse model of type 2 diabetes.
abstract: In this study we examined the mechanisms of motor dysfunction in type 2 diabetes.
  
  
  
  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.
  
  
  
  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.
  
  
  
  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.
authors.affiliation: Department of Biomedicine, Aarhus University, Building 1163, Ole Worms Allé 4, DK-8000, Aarhus C, Denmark.
authors.forename: Jeppe Seamus
authors.initials: JS
authors.lastname: Bayley
authors.affiliation: Department of Biomedicine, Aarhus University, Building 1163, Ole Worms Allé 4, DK-8000, Aarhus C, Denmark.
authors.forename: Thomas Holm
authors.initials: TH
authors.lastname: Pedersen
authors.affiliation: Department of Biomedicine, Aarhus University, Building 1163, Ole Worms Allé 4, DK-8000, Aarhus C, Denmark.
authors.forename: Ole Baekgaard
authors.identifier: 0000-0003-3535-7862
authors.initials: OB
authors.lastname: Nielsen
mesh_terms: D000255:Adenosine Triphosphate / Q000493:pharmacokinetics; D000704:Analysis of Variance; D000818:Animals; D001835:Body Weight / Q000235:genetics; D002118:Calcium / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000235:genetics; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D051379:Mice; D008817:Mice, Mutant Strains; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000187:drug effects / Q000503:physiopathology*; D009135:Muscular Diseases / Q000209:etiology* / Q000473:pathology*; D009154:Mutation / Q000235:genetics; D018733:Nicotinic Antagonists / Q000494:pharmacology; D010759:Phosphorus Isotopes / Q000493:pharmacokinetics; D054411:Receptors, Leptin / Q000235:genetics; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism; D014403:Tubocurarine / Q000494:pharmacology
chemical_list: D018733:Nicotinic Antagonists; D010759:Phosphorus Isotopes; D054411:Receptors, Leptin; D000255:Adenosine Triphosphate; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D002118:Calcium; D014403:Tubocurarine
keywords: SERCA; excitability; half-relaxation time; neuropathy; skeletal muscle; type 2 diabetes mellitus