The effect of chronic hypoxia on ketone body metabolism in brook trout (Salvelinus fontinalis)

Abstract

Hypoxic zones are detrimental to fish, and their duration is increasing due to climate change. For short-term hypoxic exposures, teleost fish may rely on anaerobic glucose metabolism via glycolysis, however given the limited glycogen stores in these animals glucose will not be sufficient to survive over the long-term. The substrate that they use to tolerate chronic hypoxic exposures is currently unknown, but amino acids, ketone bodies, or lipids are possible. Ketone bodies may be preferable due to the low oxygen cost, production efficiency, and potential anti-oxidative effects. The purpose of my research was to investigate if teleost fish are capable of metabolizing ketone bodies during exposures to chronic hypoxia. Using brook trout (Salvelinus fontinalis) as our model organism, we placed fish in 50% dissolved oxygen for 24-hours as an acute exposure and 9-days as a chronic exposure, and compared these to control fish and those that were starved for 9 days. After treatment I took blood, heart, liver, and white muscle samples and performed assays to assess ketone activity. Liver glycogen decreased significantly following chronic hypoxia, suggesting that glucose stores were depleted. The activity of β-hydroxybutyrate dehydrogenase was unaffected by exposure to hypoxia and similarly, I observed no changes in plasma β-hydroxybutyrate. However, plasma acetoacetate decreased significantly following chronic hypoxia, which may be due to increased uptake into tissues. Activity of succinyl-CoA:3-ketoacid-CoA transferase (SCOT) increased in the heart after chronic hypoxia, but SCOT was decreased in white muscle after both acute and chronic hypoxia. This suggests that ketogenic responses are tissue-specific, and that the heart may utilize ketones to maintain a steady ATP source. In conclusion, this research suggests that S. fontinalis is capable of partial ketogenic responses during chronic hypoxia and this may help to support ATP production in obligate organs like the heart.