Multiple retinoids alter liver bile salt-independent retinyl ester hydrolase activity, serum vitamin A and serum retinol-binding protein of rats

Liver bile salt-independent retinyl ester hydrolase (BSI-REH) has been suggested to play a significant role in the hydrolysis of chylomicron derived retinyl esters. Studies were conducted to investigate the individual effects of N-(4-hydroxyphenyl)retinamide (HPR), retinoic acid, 13-cis-retinoic acid, Acitretin and Temarotene on BSI-REH, serum retinol, and serum retinol-binding protein (REP) concentrations. We have demonstrated that micromofar concentrations of HPR, retinoic acid, 13-cis-retinoic acid or Acitretin significantly reduced the in vitro hydrolysis of retinyl palmitate. In contrast, Temarotene stimulated retinyl palmitate hydrolysis by BSI-REH. Retinoic acid and 13-cis-retinoic acid produced transient, but significant, depressions of both serum retinol and REP concentrations, when the individual retinoids were administered orally to rats. The duration of the depression was shorter than we previously observed with acute HPR administration. Furthermore, Acitretin appeared to function with bimodal activity, producing significant depressions of serum retinol at 2 h and 24 h. No effect of Acitretin or Temarotene on serum REP concentration was observed. The alterations observed in BSI-REH activity, serum retinol and REP concentrations provide evidence that these retinoids can alter liver retinyl ester hydrolysis, but the effects observed on serum retinol concentration can only be partially explained by the BSI-REH activity.