Sarah E. Ehrlicher
Oregon State University
16 Papers
18 Citations
Sarah E. Ehrlicher is an academic researcher from Oregon State University. The author has contributed to research in topics: Skeletal muscle & Mitochondrion. The author has an hindex of 6, co-authored 12 publications.
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Papers
Robust intrinsic differences in mitochondrial respiration and H2O2 emission between L6 and C2C12 cells
Matthew M. Robinson,Bergen K. Sather,Emily R. Burney,Sarah E. Ehrlicher,Harrison D. Stierwalt,Maria Clara Franco,Sean A. Newsom +6 more
TL;DR: L6 myoblasts had lower respiration rates than C2C12 myoblast, including lesser capacity for fatty acid oxidation and greater electron leak towards H2O2, and L6 cells also retain a lower capacity for electron transfer following differentiation to form fused myotubes.
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Long-term rates of mitochondrial protein synthesis are increased in mouse skeletal muscle with high-fat feeding regardless of insulin-sensitizing treatment.
Sean A. Newsom,Benjamin F. Miller,Karyn L. Hamilton,Sarah E. Ehrlicher,Harrison D. Stierwalt,Matthew M. Robinson +5 more
TL;DR: Mitochondrial protein synthesis and palmitoyl- l-carnitine oxidation were increased in mice consuming a high-fat diet, regardless of differences in insulin sensitivity with pioglitazone treatment, and may contribute to remodeling of the mitochondria to increase lipid oxidation capacity.
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Insulin-stimulated Rac1-GTP binding is not impaired by palmitate treatment in L6 myotubes
Harrison D. Stierwalt,Sarah E. Ehrlicher,Bryan C. Bergman,Matthew M. Robinson,Sean A. Newsom +4 more
TL;DR: It is suggested that attenuated PAK phosphorylation and impaired GLUT4 translocation during palmitate‐induced insulin resistance can occur independent of defects in insulin‐stimulated Rac1‐GTP binding, and Rac1 may not undergo negative regulation by DAG or ceramides.
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Remodeling of skeletal muscle mitochondrial proteome with high-fat diet involves greater changes to β-oxidation than electron transfer proteins in mice
TL;DR: After the 60% fat diet, remodeling of the mitochondrial proteome revealed upregulation of proteins regulating lipid oxidation that was not evident for all mitochondrial pathways, suggesting the accumulation of lipid metabolites with obesity may occur without intrinsic dysfunction to mitochondrial lipid oxidation.
Mitochondrial adaptations to exercise do not require Bcl2-mediated autophagy but occur with BNIP3/Parkin activation.
Sarah E. Ehrlicher,Harrison D. Stierwalt,Benjamin F. Miller,Sean A. Newsom,Matthew M. Robinson +4 more
TL;DR: Increases in basal mitochondrial turnover, not transient activation with exercise, mediate adaptations to exercise and high‐fat diet.
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