Incorporation of vitamin A into milk of wild type and mutant mice

Abstract

Green et al. estimated that 40–70% of vitamin A delivered to the milk of lactating rats is derived via plasma retinol-binding protein (RBP) with the rest arriving postprandially (J. Nutr. 131: 1279-82, 2001). To explore the role of RBP in this process, we assessed retinoid levels in milk of lactating RBP−/− and wild type mice consuming a chow diet fed ad lib. No statistically significant differences in milk total retinol levels were observed between the RBP−/− and wild type mice. Total retinol levels at different postpartum days for RBP−/− and wild type mice respectively were: days 1-5, 5.7 ± 2.1 μM and 10 ± 5 μM; days 6–14, 14.5 ± 4.3 μM and 9.2 ± 6.6 μM; and day 15 onward, 10.4 ± 4.2 μM and 16 ± 6.4 μM. Hence, RBP is not required for maintaining delivery of retinoids for milk production suggesting that milk vitamin A can be acquired solely from dietary retinol. RBP-/- mice incorporate higher [3H]retinol into their milk than wild type mice when measured over 6 hours postprandially, indicating a compensatory up-regulation in the mutants. We investigated the role of enzymes needed for retinyl ester hydrolysis and synthesis in facilitating retinoid incorporation into milk using mice lacking lipoprotein lipase (LpL) and mice lacking lecithin:retinol acyltransferase (LRAT). The lipase inhibitor p407 significantly reduced the incorporation of post prandial [3H]retinol into milk of the RBP-/- demonstrating the importance of this pathway. Studies of milk formation in LRAT-deficient mice indicate that LRAT is not needed for incorporation of vitamin A into milk. Our studies help define the biochemical factors that are critically needed for milk formation. (Supported by NIH grant R01 DK068437)