The effect of glucocorticosteroids on serum, liver, and lung vitamin A and retinyl ester concentrations

Vitamin A and its active metabolites are important factors in promoting normal respiratory epithelial differentiation and growth. Glucocorticoids, often used to treat chronic lung diseases in infancy and childhood, are known to increase serum retinol concentrations. To determine the effects of exogenous steroids on serum retinol and retinol-binding protein concentrations (as well as on liver and lung total vitamin A, retinol, and retinyl ester concentrations), 32 weanling Sprague-Dawley rats were divided into four equal experimental groups. Eight animals were vitamin A sufficient and received 7 days of intraperitoneal dexamethasone at 0.5 mg/kg/day (group SD), 8 were vitamin A sufficient and received placebo (group SP), 8 were made vitamin A deficient and subsequently received dexamethasone (group DD), and 8 were vitamin A deficient and received placebo (group DP). Dexamethasone increased serum retinol concentrations in the SD group (2.27 ± 0.20 μmol/L) when compared with control (SP, 1.64 ± 0.46 μmol/L, p < 0.001) as well as with pretreatment baseline values (1.21 ± 0.23 μmol/L, p < 0.001). Lung total vitamin A, retinol, and individual retinyl esters were depleted by 56 ± 19% in the SD group, whereas liver values were depleted by 36 ± 23%. In the vitamin A-sufficient groups the relative percentages of four major retinyl esters (palmitate, stearate, oleate, and linoleate) did not change in either tissue after steroid exposure. The vitamin A-deficient groups had no detectable tissue vitamin A, and dexamethasone did not increase serum retinol concentrations in the DD group. Serum retinol-binding protein concentrations were significantly higher in both steroid-treated groups when compared with control. Dexamethasone increases serum retinol and retinol-binding protein concentrations in vitamin A suffi-cient rats, apparently at the expense of both lung and liver total vitamin A, retinol, and retinyl ester concentrations. We speculate that the liver and lungs are two sources for the increase in serum retinol reported with glucocorticosteroids.