Evidence for a Pathogenic Role of ω6 Polyunsaturated Fatty Acid in the Cutaneous Manifestations of Biotin Deficiency
Evidence for a Pathogenic Role of ω6 Polyunsaturated Fatty Acid in the Cutaneous Manifestations of Biotin Deficiency
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ω6 多不饱和脂肪酸在生物素缺乏的皮肤表现中致病作用的证据
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发表时间：
1990
期刊：
影响因子：
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通讯作者：
D. Mock
中科院分区：
文献类型：
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作者：
D. Mock
在人类和大鼠生物素缺乏症中检测到脂肪酸组成异常。然而，这些异常的发病作用，如果有的话，在生物素缺乏症的皮肤表现尚不清楚。在营养素相互作用实验中，我们检验了ω6多不饱和脂肪酸（PUFA）代谢异常在皮肤表现中起致病作用的假设。5只大鼠喂食诱导生物素缺乏的鸡蛋白色饲料;这些大鼠出现生物素缺乏的特征性皮肤异常。另外5只大鼠成对喂食鸡蛋白色饲料并接受Liposyn [77%亚油酸（18：2ω6）];这些大鼠未出现生物素缺乏的皮肤表现。两组在生物素尿排泄率、血清生物素浓度、肝脏生物素含量和两种生物素依赖性羧化酶的肝脏活性方面的降低相似;两组在3-羟基异戊酸尿排泄率方面的增加相似。这些观察结果证明：（a）ω6 PUFA代谢的某些异常在生物素缺乏的皮肤表现中具有致病作用，（B）这种致病作用不能解释为由于Liposyn的生物素节约效应而导致的生物素营养状态的差异。
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 ω6 polyunsaturated fatty acid (PUFA) metabolism plays a pathogenetic role in the cutaneous manifestations. Five rats were fed an egg white diet that induces biotin 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 (18:2ω6)]; 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 hepatic activities of two biotin-dependent carboxylases; the two groups had similar increases in the rates of urinary excretion of 3-hydroxyisovaleric acid. These observations provide evidence that (a) some abnormality in ω6 PUFA metabolism has a pathogenetic role in the cutaneous manifestations of biotin deficiency and (b) this pathogenetic role can not be explained as a difference in biotin nutritional status due to a biotin-sparing effect of Liposyn.