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M. L. Garcia Cazarin; Glucose Uptake Into Rat Extraocular Muscles is Regulated by Insulin and Contractile Activity. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5822.
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The extraocular muscles (EOMs) show specific adaptations intended to fulfill the metabolic demands imposed by their constant activity. We and others have proposed that faster glucose uptake is a likely adaptive strategy in these muscles. Glucose enters muscle fibers via specific transporters (GLUT1 and GLUT4) in a process regulated by insulin and contractile activity to match metabolic supply to demand in most skeletal muscles. However, that mechanism may not apply in constantly active muscles such as EOMs, as they likely have high basal glucose uptake rates.
Therefore, Wwe tested the hypothesis that glucose uptake into EOMs is not regulated by insulin or contractile activity.
EOMs isolated from adult male Sprague Dawley rats were incubated with 100 nM insulin or made to contract with electrical stimulation; glucose uptake was then measured with 2-deoxy-d[1,2-3H]glucose. The content of GLUT1, GLUT4, phosphatidylinositol 3-kinase (PI3K), total and phosphorylated protein kinase B (Akt), total and phosphorylated glycogen synthase kinase 3 (GSK3) was analyzed by western blot.
Glucose uptake into EOMs increased 108% over the basal rate after insulin stimulation (1.2±0.3 vs. 2.5±0.3 µmol/g/h basal and insulin respectively, p=0.01) and 78% after electrical stimulation (1.3±0.2 vs. 2.4±1.4 µmol /g/h basal and electrical stimulation respectively, p=0.009). GLUT1 and GLUT4 were detectable in EOMs, indicating they use the same glucose transporters as other skeletal muscles. Akt phosphorylation was 3-fold higher in EOMs following incubation with insulin (p=0.003), but there was no change in GSK3 phosphorylation, proof that insulin signaling is similar but not identical to other muscles.
These results demonstrate that glucose uptake in EOMs is regulated by insulin and contractile activity. However, there is evidence of differences in insulin signaling, some of which may lead to failure to induce glycogen production in EOMs.Research supported by NIH grant R01 EY012998-09.
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