Riboflavin nutritional status and flavoprotein enzymes in normal and genetically diabetic KK mice

Abstract

Riboflavin nutritional status in normal control Swiss albino (SA) and genetically diabetic (KK) mice aged 8–9 mo was assessed by determining the glutathione reductase activity in erythrocyte hemolysates, with and without addition of flavin adenine dinucleotide (FAD); the ratio (activity with added FAD)/(activity without FAD) was expressed as the activity coefficient (AC). AC values from 0.9 to 1.3 were considered normal and those greater than 1.3 were regarded as evidence of riboflavin deficiency. Among SA mice, 35% were found to be riboflavin deficient. Among KK mice, 83% were riboflavin deficient. The difference in prevalance was significant ( p < 0.01). Supplementation of riboflavin to deficient KK mice returned their AC values to normal. Based upon AC values, both SA and KK mice were classified into normal (nondeficient) and riboflavin-deficient groups. Glutathione reductase (GR) activity in erythrocyte hemolysates and liver supernatants was significantly lower in both deficient SA and KK than in normal SA and KK mice. Treatment of deficient KK with riboflavin restored the enzyme activity in both preparations to normal. In contrast to the finding in erythrocytes, the hepatic GR activity was not increased by FAD in vitro either in normal or deficient mice. Hepatic mitochondrial succinate dehydrogenase (SDH) activity was significantly decreased in riboflavin-deficient KK mice. The enzyme activity was increased several-fold above normal in deficient KK mice supplemented with riboflavin. In conclusion, the data suggest that genetic diabetes increases the prevalence of riboflavin deficiency, which in turn causes a decrease in the erythrocyte and hepatic GR and hepatic SDH activities. This deficiency can be corrected by riboflavin supplementation, with subsequent augmentation of GR and SDH activities, indicating that these enzymes are dependent on the riboflavin nutritional status of the animal.