The impact of hypoxia on in vivo glucose uptake in a hypoglycemic fish, Myoxocephalus scorpius.
The mechanisms controlling carbohydrate utilization in teleost fish are poorly understood, particularly in the heart. Tissue glucose uptake and cardiovascular characteristics were measured in the short-horned sculpin, Myoxocephalus scorpius, a species exhibiting low blood glucose levels, during normoxia and hypoxia to assess the role of adenosine receptors in the control of glucose uptake and anaerobic metabolism. As expected, hypoxia exposure (300 min at 2 mg/l dissolved oxygen) resulted in a bradycardia and plasma lactate accumulation, but glucose uptake rates did not change in heart, brain, gill, spleen, and white muscle. Plasma glucose-to-intracellular glucose ratios indicated that glucose uptake was the rate-limiting step in glucose utilization. The majority of intracellular glucose was unphosphorylated, however, suggesting that hexokinase is also important in controlling the tissue glucose gradient. During hypoxia, the cholinergic blocker atropine resulted in tachycardia but did not significantly change tissue glucose uptake rates or heart and brain adenosine levels. In contrast, the combined treatment of atropine and an adenosine receptor blocker [8-(p-sulfophenyl)theophylline] during hypoxia increased heart glucose uptake to levels fivefold higher than normoxic fish, with no additive effects on cardiovascular parameters. Significant tissue lactate accumulation was observed in this group of fish, signifying that adenosine receptors may depress anaerobic metabolism, even though tissue adenosine accumulation was absent during hypoxia. White muscle accumulated glucose during normoxia, suggesting the presence of gluconeogenic pathways or active uptake mechanisms not previously described in this tissue.
MacCormack
Tyson J
TJ
Ocean Sciences Centre, Memorial University of Newfoundland, St. John's, Newfoundland, Canada. tysonmacc@ualberta.ca
Driedzic
William R
WR
D000241:Adenosine / Q000378:metabolism; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001786:Blood Glucose / Q000502:physiology*; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology; D050260:Carbohydrate Metabolism / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D003847:Deoxyglucose / Q000378:metabolism; D045604:Extracellular Fluid / Q000378:metabolism / Q000502:physiology; D005399:Fishes / Q000502:physiology*; D005947:Glucose / Q000378:metabolism*; D019298:Glucose-6-Phosphate / Q000378:metabolism; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D000860:Hypoxia / Q000378:metabolism*; D019344:Lactic Acid / Q000097:blood / Q000378:metabolism; D018727:Muscarinic Antagonists / Q000494:pharmacology; D010766:Phosphorylation; D058915:Purinergic P1 Receptor Antagonists; D013806:Theophylline / Q000031:analogs & derivatives / Q000494:pharmacology; D014018:Tissue Distribution
D001786:Blood Glucose; D018727:Muscarinic Antagonists; D058915:Purinergic P1 Receptor Antagonists; D019344:Lactic Acid; D019298:Glucose-6-Phosphate; D001285:Atropine; C031433:8-(4-sulfophenyl)theophylline; D003847:Deoxyglucose; D013806:Theophylline; D005947:Glucose; D000241:Adenosine