Abstract
Essential fatty acid deficiency has been widely studied but the extent to which its effects are attributable specifically to deficiency of linoleate as opposed to deficiency of all unsaturated fatty acids is unknown. Our objective was to evaluate the effect of pure linoleate deficiency on growth as well as changes in the metabolism and oxidation of n-6 polyunsaturates. The diets contained 20 energy % fat blended from 3 energy % pure oleate, 2 energy % linoleate (0.01 energy % in the linoleate-deficient group), 0.3 energy % pure alpha-linolenate, and the balance as palmitate and stearate from fully hydrogenated soybean oil. Thirty-five-day-old rats consumed the two diets for 84 days, after which the linoleate-deficient rats weighed 15% less than the controls (P < 0.05), had mild scaling on the paws, and visible hair loss (in a few rats). Compared with the controls, the ratio of eicosatrienoate to arachidonate after 84 days was elevated in liver (170-fold) and serum (520-fold) phospholipids of the linoleate-deficient group. In total, linoleate-deficient rats consumed 122 mg of linoleate and had a net whole body loss of 479 mg n-6 polyunsaturates compared with an intake of 24,130 mg and a net whole body gain of 7206 mg n-6 polyunsaturates in the control group. Linoleate-deficient rats oxidized 1% of an oral bolus of [1-14C]linoleate over 8 h compared with 34% in the control rats (P < 0.05). We conclude that pure linoleate deficiency has marked effects on accumulation of n-6 polyunsaturates but induces milder gross symptoms, particularly growth retardation, than classical essential fatty acid deficiency. alpha-Linolenate and possibly oleate may have a sparing effect on linoleate oxidation from body stores during linoleate deficiency.
Highlights
Essential fatty acid deficiencyhas been widely studied but the extent to which its effects are attributable to deficiency of linoleate as opposed to deficiency of all unsaturated fatty acids is unknown
Mammals consuming a diet that is either fat-free or that contains dietary fat derived exclusively from saturated fatty acids become deficient in n-6 and n-3 polyunsaturated fatty acids (PUFA)
Our objectivewas to induce pure linoleate deficiency and evaluate its effects on linoleate oxidation to determine whether body stores of linoleate were conserved when dietary linoleate was inadequate
Summary
Essential fatty acid deficiencyhas been widely studied but the extent to which its effects are attributable to deficiency of linoleate as opposed to deficiency of all unsaturated fatty acids is unknown. Deficiency, including growth retardation, scaliness of the skin, impaired water retention, impaired reproduction, and raised ratio of eicosatrienoate-arachidonate (20:3n-9/20:4n-6) in tissue lipids These symptoms are mostly attributable to the dietary absence of linoleate (18:2n-6) and to the subsequent loss of linoleate and arachidonate (20:4n-6) from membrane lipids [1,2,3,4,5]. The only diets from which it is absent are those that are EFAdeficient It is unclear which symptoms of EFA deficiency are dependent exclusively on the dietary absence of linoleate alone compared with those symptoms elicited o r exacerbated by other dietary changes, including the absence of dietary a-linolenate or oleate, effects of added cholesterol, very high saturated fat intake, fasting, etc.
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