Evidence for a Pathogenic Role of ω6 Polyunsaturated Fatty Acid in the Cutaneous Manifestations of Biotin Deficiency

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Abstract
Abnormalities in fatty acid composition have been detected in biotin deficiency in humans and in the rat. However, the pathogenetic role of these abnormalities, if any, in the cutaneous manifestations of biotin deficiency is not clear. In a nutrient interaction experiment, we tested the hypothesis that an abnormality of .omega.6 polyunsaturated fatty acid (PUFA) metabolism plays a pathogenetic role in the cutaneous manifestations. Five rats were fed an egg white diet that induces bitoin deficiency; these rats developed the characteristic cutaneous abnormalities of biotin deficiency. Five additional rats were pair-fed the egg white diet and received Liposyn [77% linoleic acid (18:20.omega.6)]; these rats did not develop the cutaneous manifestations of biotin deficiency. The two groups had similar decreases in the rates of urinary excretion of biotin, the serum concentrations of biotin, the amounts of biotin in liver, and the heptic activities of two biotin-dependent carboxylases; the two groups had similar increases in the rates of urinary excretion of 2-hydroxyisovaleric acid. These observations provide evidence that (a) some abnormality in .omega.6 PUFA metabolism has a pathogenetic role in the cutaneous manifestations of biotin deficiency and (b) this pathogenic role cannot be explained as a difference in biotin nutritional status due to a biotin-sparing effect of Liposyn.
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