Effect of chronic incubation of CaCo-2 cells with eicosapentaenoic acid (20:5, n-3) and oleic acid (18:1, n-9) on triacylglycerol production
Trine Ranheim, Ane Gedde‐Dahl, Arild C. Rustan, Christian A. Drevon
Abstract
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Trine Ranheim, Ane Gedde‐Dahl, Arild C. Rustan, Christian A. Drevon
Abstract
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CaCo-2 monolayers, cultured for 1 week after reaching confluence, were incubated with micellar solutions of fatty acids for up to 7 days. These conditioned cells were incubated acutely (5 h) with eicosapentaenoic acid and oleic acid, and the levels of cell-associated and secreted triacylglycerol were determined. With acute addition of oleic acid, both cell-associated and secreted triacylglycerol were decreased in cells chronically exposed to eicosapentaenoic acid. This effect was observed after as little as 2 days of chronic incubation with eicosapentaenoic acid. A further decrease was found when these cells were incubated acutely with eicosapentaenoic acid, regardless of which radioisotopes were used to label precursors in the incubation media. The secretion of both labelled and total triacylglycerol and apolipoprotein B was reduced approximately 50% in cells incubated chronically with eicosapentaenoic acid. The amounts of triacylglycerol and apolipoprotein B within the cells were not decreased by chronic exposure to eicosapentaenoic acid. Our data indicate that CaCo-2 cells chronically incubated with eicosapentaenoic acid secrete significantly less triacylglycerol than cells incubated chronically with oleic acid. When eicosapentaenoic acid was also included acutely, triacylglycerol secretion was reduced even more. We conclude that chronic exposure of eicosapentaenoic acid to this intestinal cell type reduces the rate of chylomicron secretion and may help explain the decreased postprandial lipaemia observed in humans taking fish oil supplements.
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CaCo-2 monolayers, cultured for 1 week after reaching confluence, were incubated with micellar solutions of fatty acids for up to 7 days. These conditioned cells were incubated acutely (5 h) with eicosapentaenoic acid and oleic acid, and the levels of cell-associated and secreted triacylglycerol were determined. With acute addition of oleic acid, both cell-associated and secreted triacylglycerol were decreased in cells chronically exposed to eicosapentaenoic acid. This effect was observed after as little as 2 days of chronic incubation with eicosapentaenoic acid. A further decrease was found when these cells were incubated acutely with eicosapentaenoic acid, regardless of which radioisotopes were used to label precursors in the incubation media. The secretion of both labelled and total triacylglycerol and apolipoprotein B was reduced approximately 50% in cells incubated chronically with eicosapentaenoic acid. The amounts of triacylglycerol and apolipoprotein B within the cells were not decreased by chronic exposure to eicosapentaenoic acid. Our data indicate that CaCo-2 cells chronically incubated with eicosapentaenoic acid secrete significantly less triacylglycerol than cells incubated chronically with oleic acid. When eicosapentaenoic acid was also included acutely, triacylglycerol secretion was reduced even more. We conclude that chronic exposure of eicosapentaenoic acid to this intestinal cell type reduces the rate of chylomicron secretion and may help explain the decreased postprandial lipaemia observed in humans taking fish oil supplements.
Key concepts: Eicosapentaenoic acid, Oleic acid, Docosahexaenoic acid, Incubation, Chylomicron, Fatty acid, Biochemistry, Internal medicine