Fish exhibit a wide range of species specific blood glucose levels. How this relates to glucose utilization is yet to be fully realized. Here we assess glucose transport and metabolism in myocytes isolated from Atlantic cod and short-horned sculpin, species with blood glucose levels of 3.7 and 0.57 mmol l−1, respectively. Glucose metabolism was assessed by the production of 3H2O from [2-3H]-glucose. Glucose metabolism was 3.5-6 fold higher by myocytes from Atlantic cod than short-horned sculpin at the same level of extracellular glucose. In Atlantic cod myocytes glucose metabolism displayed what appears to be a saturable component with respect to extracellular glucose and cytochalasin B inhibited glucose metabolism. These features revealed a facilitated glucose diffusion mechanism that accounts for between 30% and 55% of glucose entry at physiological levels of extracellular glucose. Facilitated glucose diffusion appears to be minimal in myocytes for short-horned sculpin. Glucose entry by simple diffusion occurs in both cell types with the same linear relationship between glucose metabolism and extracellular glucose concentration presumably due to similarities in membrane composition. Oxygen consumption by myocytes incubated in medium containing physiological levels of extracellular glucose (Atlantic cod 5 mmol l−1; short-horned sculpin 0.5 mmol l−1) was similar in both species and was not decreased by cytochalasin B immediately suggesting that these cells have the capability of oxidizing alternative on-board metabolic fuels. Cells produced lactate at low rates but glycogen levels did not change during the incubation period. In cells from both species, glucose utilization assessed by both simple chemical analysis of glucose disappearance from the medium and 3H2O production matched one-half the rate of lactate production and as such extracellular glucose was not available for oxidative metabolism. Overall, extracellular glucose makes only a minor contribution to ATP production but a sustained glycolysis may be necessary to support Ca2+ transport mechanism at either the sarcoplasmic reticulum or the sarcolemmal membrane.
- Received October 1, 2015.
- Accepted February 23, 2016.
- © 2016. Published by The Company of Biologists Ltd