Earlier studies have shown that retinoid administration suppresses the generation of hepatic
fibrosis and stimulates its regression in normal (ie, vitamin A-sufficient) carbon tetrachloride-
treated rats. This study focuses on the possible role of a marginal or deficient vitamin A
status on carbon tetrachloride-induced fibrosis. This experimental study in rats shows that
vitamin A status, reflected by hepatic retinoid content (retinol and retinyl esters), modulates
the development of hepatic fibrosis induced by carbon tetrachloride. In rats with low hepatic …