Abstract:
Unlike many teleosts, elasmobranchs lack a swim bladder and increase their buoyancy by storing high concentrations of lipids in their livers. However, this lipid is thought to not be used directly as a fuel, which appears to be an oddity among vertebrates and potentially energetically wasteful. For hepatic lipids to be metabolised, they appear to be converted to ketone bodies, where a considerable amount of carbon is assumed to be lost to acetone. It is also surprising that lipids are not used as a fuel as the hearts of other vertebrates are mostly dependent on lipid metabolism at low work rates. Although low, Moyes et al. (1990) reported activities of carnitine palmitoyltransferase (the lipid mitochondrial importer), and therefore elasmobranchs do still have the enzymes required for fatty acid oxidation. Previous work analysing mitochondrial metabolic function in elasmobranchs has used isolated mitochondria to determine capacities to metabolise lipid derived substrates. Mitochondrial isolation may damage mitochondria. This study aimed to revisit these previous findings with the hypothesis that elasmobranch cardiac and skeletal muscle can directly metabolise lipids, using an in situ approach of permeabilised fibres, where the cellular environment is preserved. To test this hypothesis, mitochondrial assays were undertaken to test various substrates’ (pyruvate, β-hydroxybutyrate and palmitoylcarnitine) use by cardiac and skeletal muscle mitochondria. The elasmobranchs analysed (spiny dogfish, carpet shark and school shark) were compared with mammalian (Sprague-Dawley rat) and teleost (spotted wrasse) representatives. No significant increases in average oxygen flux were observed with palmitoylcarnitine in the elasmobranch tissues, however. The respirometry results of this study mostly support previous research suggesting that elasmobranchs utilise ketone bodies rather than lipids in both cardiac and skeletal muscle.