De novo lipogenesis in Atlantic salmon adipocytes

•The capacity of fish adipocytes to convert glucose into fatty acids by DNL is low.•The limited capacity of DNL may contribute to glucose intolerance in fish.•Salmon adipocytes mainly transform glucose to glycerol and Krebs-cycle intermediates.•Glycolysis, PPP and glyceroneogenesis can provide cofactors for lipid metabolism.

BackgroundCarnivorous teleost fish utilize glucose poorly, and the reason for this is not known. It is possible that the capacity of adipocytes to synthesize lipids from carbohydrate precursors through a process known as “de novo lipogenesis” (DNL) is one of the factors that contributes to glucose intolerance in Atlantic salmon.MethodsPrimary adipocytes from Atlantic salmon differentiated in vitro were incubated with radiolabelled glucose in order to explore the capacity of salmon adipocytes to synthesize and deposit lipids from glucose through DNL. The lipid-storage capacity of adipocytes incubated with glucose was compared with that of cells incubated with the fatty acid palmitic acid. Quantitative PCR and immunohistochemistry were used to assess changes of genes and proteins involved in glucose and lipid transport and metabolism.ResultsLess than 0.1% of the radiolabelled glucose was metabolized to the fatty acids 16:0 and the stearoyl-CoA desaturase products 16:1 and 18:1 by DNL, whereas approximately 40% was converted to glycerol to form the triacylglycerol backbone of lipids. Transcriptional analysis indicated that adipocytes ensure the availability of necessary cofactors and other substrates for lipid synthesis and storage from glycolysis, the pentose phosphate pathway and glyceroneogenesis.ConclusionsWe have shown for the first time that the DNL pathway is active in fish adipocytes. The capacity of the pathway to convert glucose into cellular lipids for storage is relatively low.General significanceThe limited capacity of adipocytes to utilize glucose as a substrate for lipid deposition may contribute to glucose intolerance in salmonids.