ACUTE-INFLAMMATION INDUCES HYPORETINEMIA AND MODIFIES THE PLASMA AND TISSUE-RESPONSE TO VITAMIN-A SUPPLEMENTATION IN MARGINALLY VITAMIN-A-DEFICIENT RATS

Plasma retinol is reduced during numerous infections, and inflammation alters the hepatic synthesis of retinol-binding protein (RBP). In thi s study, we have investigated the effects of endotoxin-induced inflamm ation on vitamin A (VA) supplementation in a rat model of marginal VA deficiency. Marginally VA-deficient rats received an intraperitoneal d ose of lipopolysaccharide (LPS, n = 14) or saline (n = 10); 6 h later, six LPS + VA and six saline + VA rats received 7.1 mu mol VA orally. Twenty-four hours after endotoxin administration, rats with inflammati on (LPS) had lower plasma retinol, RBP, and hepatic RBP than saline ra ts (37, 31 and 44%, respectively, P < 0.05). Inflammation did not affe ct VA concentrations in liver and perirenal adipose tissue, although k idney VA was reduced relative to saline rats. However, urinary VA was not detected. Eighteen hours after VA supplementation, inflammation re duced the plasma unesterified retinol response (P < 0.05) in LPS + VA relative to saline + VA rats, although total VA increased as a result of the presence of retinyl esters in LPS + VA rats. Hepatic esterified retinol concentration was reduced (P < 0.01) in LPS + VA compared wit h saline + VA rats; however, hepatic unesterified retinol did not diff er. Renal total retinol increased in VA-supplemented rats, but urinary retinol excretion, when observed, was low, independently of inflammat ion. These findings indicate that inflammation-induced hyporetinemia d oes not necessarily imply a loss of VA, but rather represents a redist ribution of tissue VA brought about by a reduced hepatic synthesis of RBP. Practical implications from these collective results are to recom mend the determination of both unesterified and esterified retinol to fully assess the plasma response to VA supplementation and to caution the use of VA assessment methodologies that depend on the hepatic synt hesis of RBP during acute inflammation.