Abstract

A significant portion of the β-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.

Highlights

  • A significant portion of the ␤-oxidized carbon skeleton of some polyunsaturated fatty acids can be recycled into de novo lipogenesis, i.e., cholesterol, saturates and monounsaturates

  • Tissue fatty acid profiles, and 14C excretion in breath of these animals have previously been reported [1]; the present report addresses 14C in fecal and liver lipids as they relate to evidence for carbon recycling from [1-14C]linoleate

  • Using rats made and severely linoleate deficient, our primary aim was to quantify the recycling of carbon from [14C]linoleate in liver lipids

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Summary

Introduction

A significant portion of the ␤-oxidized carbon skeleton of some polyunsaturated fatty acids can be recycled into de novo lipogenesis, i.e., cholesterol, saturates and monounsaturates. Despite severe depletion of n–6 polyunsaturates from body stores [1], pure linoleate deficiency from shortly after weaning causes less severe growth retardation and other gross symptoms than provision of an essential fatty acid deficient or fat-free diet [2, 3, 5]. These studies suggest that essential fatty acid deficiency is not synonymous with linoleate deficiency and may overestimate the true requirement for linoleate per se [1, 5]. Involved a multiple, non-specific deficiency of unsaturated 18 carbon fatty acids from three distinct fatty acid families (linoleate, ␣-linolenate, oleate)

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