Lipid metabolism in riboflavin-deficient rats

1. The increase in activation coefficient (stimulated: basal activity) of erythrocyte NAD(P)H 2 :glutathione oxidoreductase ( EC 16.4.2) 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. 2. Their gain in body-weight was, however, 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. 3. 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 ω6 and the decrease in proportion of 20:4 ω6 observed in deficient animals were due specifically to riboflavin deficiency, whereas certain other changes were probably caused by inanition. The changes in 18:2ω6 and 20:4 ω6 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. 4. A consistent increase in proportion of 18:2 ω6 was also observed in the hepatic triglycerides, together with a decrease in proportion of 16:0. 5. It is concluded that acute riboflavin deficiency affects lipid metabolism in a characteristic manner, probably by interfering with β-oxidation of fatty acids, but that diets of high lipid content do not significantly increase the extent of flavin depletion.