The Role of MicroRNA-26a In Skeletal Muscle Insulin Signaling
1 online resource (55 pages) : PDF
University of North Carolina at Charlotte
Chronic saturated fatty acid exposure causes skeletal muscle cells to develop insulin resistance, which contributes to the pathogenesis of type 2 diabetes mellitus. Recently, microRNAs have been viewed as novel molecules that contribute to the regulation of insulin responsiveness when cells are challenged with fatty acids. The aim of the present study was to identify the role of miR-26a in skeletal muscle cells insulted with a chronic exposure of palmitic acid (PA). A C2C12 cell culture model was utilized and protein and RNA expression was evaluated using Western blot analysis and real time polymerase chain reaction, respectively. The results of our study indicate that PA reduces insulin responsiveness in myoblasts through reductions in total and phosphorylated protein kinase B (AKT). Reduced phosphorylated AKT is suggestive of diminished glucose uptake ability and other insulin-sensitive processes. Additionally, we observed that overexpressing miR-26a was not able to alleviate the decreased signaling caused by chronic PA treatment. In conclusion, our study identified that miR-26a may not have a central role in regulating PA-induced insulin resistance in myoblasts. However, the impaired insulin response in myoblasts observed in our study eludes to a disruption in the myogenic program through AKT, which may have negative implications in muscle growth and regeneration, as well as contributing to glucose intolerance.
INSULIN SIGNALINGMICRORNAMIR-26AMYOBLASTPALMITIC ACIDSKELETAL MUSCLE
Arthur, SusanTurner, MichaelAfonin, Kirill
Thesis (M.S.)--University of North Carolina at Charlotte, 2018.
This Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s). For additional information, see http://rightsstatements.org/page/InC/1.0/.
Copyright is held by the author unless otherwise indicated.