LIPID-METABOLISM IN RIBOFLAVIN-DEFICIENT RATS .1. EFFECT OF DIETARY LIPIDS ON RIBOFLAVIN STATUS AND FATTY-ACID PROFILES
LIPID-METABOLISM IN RIBOFLAVIN-DEFICIENT RATS .1. EFFECT OF DIETARY LIPIDS ON RIBOFLAVIN STATUS AND FATTY-ACID PROFILES
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DOI：
10.1079/bjn19820069
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发表时间：
1982-01-01
影响因子：
3.6
通讯作者：
BATES, CJ
中科院分区：
文献类型：
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作者：
OLPIN, SE;BATES, CJ
在核黄素缺乏的断奶大鼠中发生的红细胞NAD（P）H：谷胱甘肽氧化还原酶（EC 1.6.4.2）的活化系数（刺激的：基础活性）增加和肝脏黄素浓度降低不受饮食中脂质浓度差异或饮食脂质中饱和或多不饱和脂肪酸总比例差异的显著或一致影响。当膳食脂质浓度从30 g/kg增加到200 g/kg时，其体重增加减少，肝脏：体重和肝脏甘油三酯含量相应增加，表明缺乏动物中高脂肪摄入的功能有害作用。当饲料中含有棉籽油时，这种情况尤其严重，棉籽油似乎对缺乏的动物有毒。缺乏、成对喂养和随意喂养的对照动物的肝磷脂的脂肪酸谱之间的比较表明，在缺乏动物中观察到的18：2 ω 6比例的增加和20：4 ω 6比例的降低特别是由于核黄素缺乏，而某些其他变化可能是由饥饿引起的。在低和高水平的脂质摄入以及低和高水平的膳食脂质多不饱和度下均观察到18：2 ω 6和20：4 ω 6的变化。在肾脏、红细胞膜和血浆磷脂中观察到脂肪酸谱的类似变化，但在心脏磷脂中未观察到。在肝甘油三酯中观察到18：2 ω 6比例的一致增加，以及16：0比例的降低。急性核黄素缺乏症以特征性方式明显影响脂质代谢，可能是通过干扰β-氧化的脂肪酸，但高脂含量的饮食并没有显着增加的程度，黄素消耗。
The increase in activation coefficient (stimulated: basal activity) of erythrocyte NAD(P)H:glutathione oxidoreductase (EC 1.6.4.2) and reduction in hepatic flavin concentration which occurred in riboflavin-deficient weanling rats were not markedly or consistently affected by differences in the concentration of lipid in the diet nor by differences in the total proportion of saturated or polyunsaturated fatty acids in the dietary lipid. Their gain in body weight was reduced when the dietary lipid concentration was increased from 30 to 200 g/kg and liver:body weight and hepatic triglyceride content were correspondingly increased, suggesting a functionally-deleterious effect of high fat intake in the deficient animals. This was especially severe when the diets contained cottonseed oil, which appeared to be toxic for the deficient animals. Comparisons between fatty acid profiles of hepatic phospholipids of deficient, pair-fed and ad lib fed control animals indicated that the increase in proportion of 18:2 .omega.6 and the decrease in proportion of 20:4 .omega.6 observed in deficient animals were due specifically to riboflavin deficiency, whereas certain other changes were probably caused by inanition. The changes in 18:2 .omega.6 and 20:4 .omega.6 were observed at both low and high levels of lipid intake and at both low and high levels of dietary lipid polyunsaturation. Similar changes in fatty acid profiles were observed in renal, erythrocyte membrane and plasma phospholipids, but were not seen in cardiac phospholipids. A consistent increase in proportion of 18:2 .omega.6 was observed in the hepatic triglycerides, together with a decrease in proportion of 16:0. Acute riboflavin deficiency apparently affects lipid metabolism in a characteristic manner, probably by interfering with .beta.-oxidation of fatty acids, but that diets of high lipid content do not significantly increase the extent of flavin depletion.