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Increased neonatal mortality in mice lacking cellular retinol-binding protein II
Xueping E1, Liang Zhang, Jianyun Lu
1Department of Medicine, Washington University, St. Louis School of Medicine, St. Louis, Missouri 63110, USA.
The Journal of Biological Chemistry
|July 26, 2002
Summary
Cellular retinol-binding protein II (CRBP II) is crucial for vitamin A transport. CRBP II deficiency impairs fetal vitamin A delivery, leading to neonatal mortality when maternal vitamin A is limited.
Area of Science:
- Biochemistry
- Molecular Biology
- Developmental Biology
Background:
- Cellular retinol-binding protein II (CRBP II) is predominantly expressed in the small intestine.
- CRBP II plays a role in retinol metabolism and transport.
Purpose of the Study:
- To investigate the physiological role of CRBP II in vivo.
- To determine the impact of CRBP II deficiency on vitamin A homeostasis and reproductive outcomes.
Main Methods:
- Gene targeting to create CRBP II knockout (CRBP II-/-) mice.
- Analysis of intestinal retinol uptake, hepatic vitamin A stores, and reproductive performance.
- Immunostaining to localize maternal CRBP II expression.
Main Results:
- CRBP II-/- mice exhibited impaired saturable intestinal retinol uptake.
- Knockout mice on a vitamin A-enriched diet had reduced hepatic vitamin A stores but normal growth and reproduction.
- CRBP II deficiency led to 100% neonatal mortality under marginal maternal vitamin A supply.
- Maternal CRBP II was detected in the placenta and small intestine.
Conclusions:
- CRBP II is essential for efficient intestinal retinol absorption.
- Both maternal and fetal CRBP II are critical for adequate vitamin A transfer to the fetus during periods of dietary restriction.
- CRBP II deficiency poses a significant risk for neonatal survival under suboptimal vitamin A conditions.