Serum vitamin A homeostasis was studied in rats with nonfiltering kidneys prepared by ligation of renal arteries. Within 1-2 h of acute renal failure, the serum retinol levelincreased by 11-73 % and was maintained for at least 4 h. More than 90 % of the increasein serum retinol was associatedwith retinolin the retinolbinding protein-transthyretin(RBP-TTR) complex. The activities ofacyl-CoA:retinol acyltransferase and retinyl-palmitate hydrolasewere not alteredby short-term acute renal failure.Oral administrationof 3H-labeledretinol3 h beforesurgeryresultedin350 % more tritiumintheserum retinol-RBP-TTR complex of rats with acute renal failure as compared to sham-operated rats; this increase represented the fraction of retinol in RBP-TTR contributed by hepatic retinol from newly absorbed 3Hlabeledretinol.Totalretinolin the retinol-RBP-TTR complex was increased by only 60%. We conclude that short-term acute renal failure causes rapid upregulation of serum retinol-RBP-TTR; the extent of the increase depends on the magnitude of hepatic vitamin A stores, particularlythe retinolpools.We hypothesizethatkidney modulates the regulationof hepatic releaseof retinol-RBP from the pool of newly acquired retinol.
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