Inflammation‐induced hyporetinolemia reduced vitamin A stores in the lungs, but not in the liver or eyes of marginally vitamin A‐deficient and ‐sufficient rats

Abstract

We assessed the consequences of prolonged-hyporetinolemia on the distribution of hepatic and extrahepatic (lungs and eyes) tissues. Vitamin A-deficient (VAD, n=8), marginally-deficient (VAM, n=14) and sufficient (VAS, n=11) male Sprague-Dawley rats received recombinant human interleukin-6 (rhIL-6) or PBS (control) continuously for 3 or 7 d. Plasma, eyes, lungs and livers were collected and retinol and retinyl palmitate (RP) were measured. Hyporetinolemia was induced by rhIL-6, and plasma retinol remained approximately 65% reduced compared to controls (P < 0.001). After 3 d of inflammation, hepatic retinol in rhIL-6-treated rats was significantly higher than in controls, independent of vitamin A status. In contrast, rhIL-6- induced-hyporetinolemia decreased retinol in both the lungs and eyes (P < 0.05), especially in VAD and VAM rats. Moreover, vitamin A stores (i.e., RP) in the lungs were lower than in controls (P < 0.05), whereas in the liver and eyes, it increased (P < 0.05). In conclusion, rhIL-6-induced-hyporetinolemia caused an increase in hepatic retinol and a concomitant reduction of retinol in extrahepatic tissues. Additionally, vitamin A-deficiency aggravated the effect of hyporetinolemia especially in the lungs. NIH NIDDK RO3DK062166