Riboflavin-deficient chicken embryos: hypoglycemia without dicarboxylic aciduria.
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.
Abrams
V A
VA
Department of Chemistry and Biochemistry, University of Delaware, Newark 19716, USA.
Han
C C
CC
White
H B
HB
D000818:Animals; D002642:Chick Embryo; D004625:Embryo, Nonmammalian / Q000378:metabolism*; D007003:Hypoglycemia / Q000378:metabolism; D012257:Riboflavin Deficiency / Q000378:metabolism*