Supplemental material for "Metabolic fuel selection in rainbow trout: Coping with Intralipid infusion"

The impact of hyperlipidemia on fuel selection has never been investigated in fish. This study quantifies how Intralipid administration affects: (i) in vivo mobilization of lipids (lipolytic rate: Ra glycerol) and carbohydrates (hepatic glucose production: Ra glucose) in rainbow trout, and (ii) key proteins involved in the regulation of fuel metabolism that could explain changes in glycerol and glucose kinetics. Results show that Intralipid triples lipolytic rate (from 2.5 ± 0.5 to 7.8 ± 1.1 µmol glycerol kg−1 min−1) and inhibits glucose production by 36% (from 7.3 ± 0.9 to 4.7 ± 0.4 µmol kg−1 min−1). The stimulation of lipolysis is probably driven by lipase activation (gene expression of hormone sensitive lipase increases in muscle), or by mass action effect. Such a strong lipolytic response is quite surprising because baseline Ra glycerol is already particularly high in fish, and well known for its stability under a variety of stresses that have important effects in mammals. The reduction in trout Ra glucose is likely caused by a large decrease in glycogen mobilization because hepatic gluconeogenic pathway capacity may rise as a consequence of increases in gluconeogenesis gene transcript levels. In contrast to humans, which maintain steady glucose production in response to Intralipid infusion, rainbow trout appear to overcompensate increased gluconeogenic capacity with a disproportionately large inhibition of glycogen breakdown. Overall, these Intralipid-driven changes in glycerol and glucose kinetics allow fish to decrease their reliance on carbohydrates and amino acids by replacing them, in part, with fatty acids as metabolic fuels.