Journal
ENDOCRINOLOGY
Volume 146, Issue 10, Pages 4479-4490Publisher
ENDOCRINE SOC
DOI: 10.1210/en.2005-0158
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Funding
- NIDDK NIH HHS [R01 DK061459-02, R01 DK061459-04, R01 DK061459-08, R01 DK061459-05, R01 DK061459-07S1, DK052444, DK068437, R01 DK061459-09, R01 DK061459, R56 DK082963-01, R01 DK061459-06, R56 DK082963, R01 DK061459-03, R01 DK061459-07, R01 DK061459-01A1S1, R01 DK061459-01A1] Funding Source: Medline
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Circulating retinoids (vitamin A and its derivatives) are found predominantly as retinol bound to retinol-binding protein (RBP), which transports retinol from liver stores to target tissues, or as retinyl ester incorporated in lipoproteins of dietary origin. The transport of retinoids from maternal to fetal circulation is poorly understood, especially under conditions of inadequate dietary vitamin A intake. Here we present RBP-/- mice as a tunable model of embryonic vitamin A deficiency. This model has enabled us to analyze metabolic links between maternal nutrition and retinoid delivery to the fetus. Our data show that retinol-RBP is the primary contributor to fetal development, whereas retinyl ester are largely responsible for accumulation of fetal retinoid stores. Furthermore, these studies indicate the importance of embryonic RBP in distributing vitamin A to certain developing tissues under restrictive diets. We also show differences among developing tissues in their dependency on the embryonic retinol-RBP pathway. Finally, we demonstrate that accumulation of embryonic vitamin A stores does not depend on the expression of RBP in the fetal liver.
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