Effects of Riboflavin Deficiency on Hepatic Gene Expression of Rats

Abstract

The prevalence of impaired riboflavin status has been around 15% to 20% across various age groups in Taiwan. In order to explore the influence of riboflavin deficiency on hepatic biochemical indices and gene expression, 60 male weanling SD rats were randomly assigned to riboflavin adequate‐ad lib, adequate‐pair fed, deficient‐ad lib and deficient‐high fat AIN‐93G diet for 3, 6 and 12 weeks after 1 week of acclimation. Riboflavin status of animals was confirmed by erythrocyte glutathione reductase activity coefficient (EGRAC) every other week. In addition to suppressed growth, riboflavin deficiency significantly reduced the liver contents of cofactors FAD and FMN, thus the enzyme activities of PMP oxidase and succinate dehydrogenase, but not glutathione reductase. Six weeks of riboflavin deficiency also resulted in changes in expression of clusters of genes responsible for energy metabolism, nutrient metabolism (methionine, iron and pyridoxine), cell cycle, apoptosis and detoxification (Cytochrome P450, family 2b and 4a, FMO, GST and UGT), analyzed by Agilent Rat Whole Genome Oligo. Therefore many changes in physiological functions of liver due to riboflavin deficiency may be regulated at transcriptional level. [Sponsored by Fu Jen University Research Grant 109631060991‐1]