| Summary: | 碩士 === 輔仁大學 === 營養科學系 === 98 === Marginal and deficient riboflavin status has been prevalent in Taiwan. In eukaryotic cells, riboflavin participates in a range of metabolic redox reactions in its coenzyme forms. The objectives of our study were 1) to establish the chronic B2 deficiency animal model, 2) to measure the effects of B2 deficiency on B2-dependent biochemical indicators, 3) to investigate the changes in gene expression due to B2 status by microarray analysis. Sixty 3-weeks-old weanling male Sprague-Dawley rats were allocated to one of the four treatment regiments, being fed either a riboflavin-adequate diet (control) ad lib, riboflavin adequate diet (pair-fed), riboflavin-deficiency diet ad lib, or riboflavin deficiency with 20 % (wt/wt) fat diet (ad lib) for 3, 7 and 12 weeks to establish the chronic riboflavin-deficient animal models. Riboflavin status was checked by erythrocyte glutathione reductase activation coefficient (EGRAC) every other week. Food intake, growth rate and the pathological signs were proportional to riboflavin content. Lower levels of organ riboflavin contents and higer EGRAC were observed in B2 deficiency and high fat groups. The activites of heart glutathione reuctase, hepatic and heart pyridoxamine (pyridoxine) 5’-phosphate oxidase, hepatic and renal succinate dehydrogenase were significantly lower in riboflavin-deficient groups than in riboflavin-adequate groups. Moreover, riboflavin deficiency alone was associated with changes in expression of clusters of genes that play roles in energy metabolism, nutrients metabolism, cell cycle progression and detoxification systems. Riboflavin deficiency with calorie-restriction was associated with changes in expression of clusters of genes involved in energy metabolism, detoxification systems, cell structures and immune systems. Riboflavin deficiency with high fat diet was associated with changes in expression of clusters of genes in energy metabolism, apoptosis, nervous systems and oxidative stress. Combination of riboflavin deficiency, calorie-restriction and high fat affected the genes expression of energy metabolism, cell cycle progression, nervous systems, detoxification systems and aging. We concluded that riboflavin deficiency resulted in changes in enzyme activities and a widespread gene expression of rat livers.
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