Original Article

Substantial carbon recycling from linoleate into products of de novo lipogenesis occurs in rat liver even under conditions of extreme dietary linoleate deficiency

Correspondence to: S. C. Cunnane.

A significant portion of the ß-oxidized carbon skeleton of some polyunsaturated fatty acids can be recycled into de novo lipogenesis, i.e., cholesterol, saturates and monounsaturates. The recycling of carbon from linoleate was quantified in liver lipids of severely linoleate-deficient rats to determine whether it is more likely to be a function of redundancy or could be obligatory. After 13 wk on a control (2 energy % linoleate) or severely linoleate-deficient (<0.05 energy % linoleate) diet, 7 µCi [1-¹⁴C]linoleate was given by gavage and the rats were killed 48 h later. A second linoleate-deficient group received an oral bolus of 256 mg linoleate as a supplement with the radiotracer. In comparison to the controls, ¹⁴C recovery in liver total lipids of the linoleate deficient group was increased about 5-fold with increased dpm/g in linoleate (13.7-fold higher), arachidonate (2.7-fold higher) and products of de novo lipogenesis (3.5-fold higher). In livers of control rats, ¹⁴C distribution was: 41% arachidonate, 29% linoleate, 22% sterols, 3% oleate, 3% palmitate, and 2% stearate. In livers of linoleate-deficient rats, ¹⁴C distribution was: 63% linoleate, 19% arachidonate, 11% sterols, 4% oleate, 3% palmitate, and <1% stearate. Thus, in controls, equivalent amounts of ¹⁴C were in products of de novo lipogenesis as in linoleate (29–30%), and in livers of linoleate-deficient rats, a similar proportion of ¹⁴C was in products of de novo lipogenesis as was converted to arachidonate (18–19%).

We conclude that carbon recycling into de novo lipogenesis accounts for a significant, obligatory component of linoleate metabolism even during extreme linoleate deficiency.—Cunnane, S. C., K. Belza, M. J. Anderson, and M. A. Ryan. Substantial carbon recycling from linoleate into products of de novo lipogenesis occurs in rat liver even under conditions of extreme dietary linoleate deficiency. J. Lipid Res. 1998. 39: 2271–2276.

Supplementary key words: linoleate, cholesterol, carbon-14, arachidonate, lipogenesis, essential fatty acid deficiency, palmitate, polyunsaturates, ß-oxidation

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