Acute Elevated Glucose Promotes Abnormal Action Potential-Induced Ca2+ Transients in Cultured Skeletal Muscle Fibers
| Autor: | Martin F. Schneider, Erick O. Hernández-Ochoa, Quinton Banks |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Time Factors Article Subject Endocrinology Diabetes and Metabolism Muscle Fibers Skeletal Action Potentials chemistry.chemical_element Calcium Biology lcsh:Diseases of the endocrine glands. Clinical endocrinology Mice 03 medical and health sciences 0302 clinical medicine Endocrinology Internal medicine medicine Animals Calcium Signaling Myopathy Cells Cultured Excitation Contraction Coupling Calcium signaling Calcium metabolism lcsh:RC648-665 Dose-Response Relationship Drug Skeletal muscle Mice Inbred C57BL Coupling (electronics) Dose–response relationship Glucose 030104 developmental biology medicine.anatomical_structure chemistry medicine.symptom 030217 neurology & neurosurgery Intracellular Research Article |
| Zdroj: | Journal of Diabetes Research Journal of Diabetes Research, Vol 2017 (2017) |
| ISSN: | 2314-6745 |
| DOI: | 10.1155/2017/1509048 |
| Popis: | A common comorbidity of diabetes is skeletal muscle dysfunction, which leads to compromised physical function. Previous studies of diabetes in skeletal muscle have shown alterations in excitation-contraction coupling (ECC)—the sequential link between action potentials (AP), intracellular Ca2+release, and the contractile machinery. Yet, little is known about the impact of acute elevated glucose on the temporal properties of AP-induced Ca2+transients and ionic underlying mechanisms that lead to muscle dysfunction. Here, we used high-speed confocal Ca2+imaging to investigate the temporal properties of AP-induced Ca2+transients, an intermediate step of ECC, using an acute in cellulo model of uncontrolled hyperglycemia (25 mM, 48 h.). Control and elevated glucose-exposed muscle fibers cultured for five days displayed four distinct patterns of AP-induced Ca2+transients (phasic, biphasic, phasic-delayed, and phasic-slow decay); most control muscle fibers show phasic AP-induced Ca2+transients, while most fibers exposed to elevated D-glucose displayed biphasic Ca2+transients upon single field stimulation. We hypothesize that these changes in the temporal profile of the AP-induced Ca2+transients are due to changes in the intrinsic excitable properties of the muscle fibers. We propose that these changes accompany early stages of diabetic myopathy. |
| Databáze: | OpenAIRE |
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