Skeletal muscle dysfunction in the db/db mouse model of type 2 diabetes

Muscle & Nerve
Jeppe Seamus BayleyOle Baekgaard Nielsen

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.

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Citations

Oct 21, 2016·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Sorabh Sharma, Rajeev Taliyan
Nov 11, 2017·Journal of Neuroengineering and Rehabilitation·Aline A GomesIsabel C N Sacco
Jan 3, 2020·Critical Reviews in Clinical Laboratory Sciences·Solaleh EmamgholipourReza Meshkani
Feb 6, 2020·Cytoskeleton·Gerardo RomanelliJuan C Benech
Sep 25, 2021·Physiological Reports·Yoshihiro TakadaSusumu Sakata
Sep 17, 2021·Diabetes Research and Clinical Practice·Maria Ruth B Pineda-CortelMiguel Francisco B Abulencia
Sep 8, 2021·Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research·Wen-Xiong LiYan Zhang

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