RIBOFLAVIN-DEFICIENT CHICKEN EMBRYOS - HYPOGLYCEMIA WITHOUT DICARBOXYLIC ACIDURIA
RIBOFLAVIN-DEFICIENT CHICKEN EMBRYOS - HYPOGLYCEMIA WITHOUT DICARBOXYLIC ACIDURIA
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DOI：
10.1016/0305-0491(94)00247-r
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发表时间：
1995-06-01
影响因子：
2.2
通讯作者：
WHITE, HB
中科院分区：
文献类型：
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作者：
ABRAMS, VAM;HAN, CC;WHITE, HB
母鸡下的蛋如果在基因上不能将核黄素沉积到蛋中，那么鸡胚胎在孵化的第13天左右就会死亡。我们发现，这些缺乏核黄素的胚胎直到死亡那天都能正常生长，而且它们的心率在死亡前一小时内都很正常。胚胎有脂肪酸氧化受损的症状，包括肝和心脏中fad依赖性中链酰基辅酶a脱氢酶活性下降，同时脂肪酸氧化中间体（C10、C12和C14酸）显著积累。与缺乏核黄素的哺乳动物不同，胚胎不会积累由脂肪酸氧化产生的二羧酸。血糖在第10天接近正常，但在死亡时降至无法检测到的水平。11天或更大的核黄素缺乏胚胎的尿囊液中乳酸含量高于3-羟基丁酸盐，而正常胚胎的情况正好相反。没有发现明显数量的甘氨酸共轭酸。我们得出结论，核黄素缺乏对鸡胚胎的主要病理影响是脂肪酸β -氧化的损害，随后有限碳水化合物储备的消耗导致猝死。
Chicken embryos in eggs laid by hens that are genetically unable to deposit riboflavin into their eggs die on or about the 13th day of incubation. We show that these riboflavin-deficient embryos grow normally until the day of death and that their heart rate is normal to within an hour of death. The embryos have symptoms of impaired fatty acid oxidation, including decreased activity of FAD-dependent medium-chain acyl CoA dehydrogenase in liver and heart along with a significant accumulation of intermediates of fatty acid oxidation (C10, C12, and C14 acids). Unlike riboflavin-deficient mammals, the embryos do not accumulate dicarboxylic acids derived from omega-oxidation of fatty acids. Blood glucose is near normal on day 10 but declines to undetectable levels by the time of death. Allantoic fluid from the riboflavin-deficient embryos of 11 days or older contains more lactate than 3-hydroxybutyrate, while in normal embryos the reverse is true. No appreciable amounts of glycine-conjugated acids were found. We conclude that the major and perhaps primary pathological effect of riboflavin deficiency in chicken embryos is the impairment of fatty acid beta-oxidation, and that the subsequent depletion of limited carbohydrate reserves leads to sudden death.