Glucose transport by English sparrow (Passer domesticus) skeletal muscle: Have we been chirping up the wrong tree?

Glucose uptake by mammalian skeletal muscle has been extensively covered in the literature, whereas the uptake of glucose by avian skeletal muscle has yet to be examined. As skeletal muscle provides the majority of postprandial glucose uptake in mammals, this study was designed to characterize the glucose transport mechanisms and glycogen content of avian skeletal muscle. In addition, plasma glucose levels were measured. English sparrow extensor digitorum communis (EDC) skeletal muscles were used for this study to quantify in vitro radiolabeled-glucose uptake. Uptake of labeled glucose was shown to decrease in the presence of increasing unlabeled glucose and was maximal by 60 minutes of incubation. Various agents known to increase glucose transport in mammalian tissues, via the insulin and contraction-responsive pathways, were used to manipulate and characterize in vitro transport in birds. The typical effectors of the mammalian insulin pathway, insulin (2 ng/ml) and insulin-like growth factor-1 (48 ng/ml), did not increase skeletal muscle glucose transport. Likewise, inducers of the mammalian contraction-responsive pathway had no effect on glucose transport by in vitro avian skeletal muscle (5 mM caffeine, 2 mM AICAR (5′-aminoimidazole-4-carboxamide-1-b-D-ribofuranoside). Interestingly, 200 μM phloretin, an agent used to block glucose transport proteins, significantly inhibited its uptake (P < 0.001). These results suggest that a glucose transporter is responsible for glucose uptake by avian skeletal muscle, albeit at unexpectedly low levels, considering the high plasma glucose concentrations (265.9 ± 53.5 mg/dl) and low skeletal muscle glycogen content (9.1 ± 4.11 nM glucose/mg) of English sparrows.