Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Lespine, A. et al.

Decreases in retinol and retinol-binding protein during total parenteral nutrition in rats are not due to a vitamin A deficiency.

Perfusion feeding in rats induced a decrease in circulating retinol despite an adequate supply of vitamin A. We studied the effect of total parenteral nutrition (TPN) on the retinol specific carrier in rat, analyzing holo-RBP (bound to retinol) and apo-RBP (without retinol) in serum and in liver. Vitamin A-sufficient (A+) and -deficient (A-) rats were characterized in terms of vitamin A and RBP status and then perfused (TPN-A+ and TPN-A-) or orally pair-fed (O-A+ and O-A-) with vitamin A. In A+ rats, a decrease in serum retinol (2.6-fold) and an increase in apo-RBP was concomitant with a massive accumulation of RBP in the liver. In TPN-A rats, both circulating RBP and liver total RBP were decreased. In TPN-A+ rats, there was a decrease in circulating retinol (2.4-fold) in parallel to a decrease of serum and liver RBP protein and mRNA. We provide evidence that infused retinyl palmitate was not responsible for serum retinol and RBP decrease and that retinol depletion was not due to vitamin A deficiency. Whatever the vitamin A status, TPN may induce in rats a down-regulation of hepatic RBP synthesis, which may, at least partially, explain the alteration of retinol and RBP in serum.[1]

References

Decreases in retinol and retinol-binding protein during total parenteral nutrition in rats are not due to a vitamin A deficiency. Lespine, A., Periquet, B., Jaconi, S., Alexandre, M.C., Garcia, J., Ghisolfi, J., Thouvenot, J.P., Siegenthaler, G. J. Lipid Res. (1996) [Pubmed]

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