Pregnancy and maternal iron deficiency stimulate hepatic CRBPII expression in rats |
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| Institution: | 1. Clincial Immunology and Allergy Unit, Department of Medicine Solna, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden;2. Department of Clinical Science and Education, Karolinska Institutet, and Sachs’ Children and Youth Hospital, Södersjukhuset, Stockholm, Sweden;3. Department of Cell and Molecular Biology and Pathogenic Bioagents, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil;1. Park Nicollet Osteoporosis Center and Institute for Research and Education, Minneapolis, MN, USA and Division of Health Policy and Management, University of Minnesota, Minneapolis, MN, USA;2. Beth Israel Deaconess Medical Center, Boston, MA, USA;3. Department of Medicine, University of Chicago, Chicago, IL, USA;4. Department of Epidemiology, Graduate school of Public Health, University of Pittsburgh, Pittsburgh, PA, USA;5. San Francisco Coordinating Center, California Pacific Medical Center, San Francisco, CA, USA;6. Division of Epidemiology and Biostatistics, University of California at San Francisco, San Francisco, CA, USA;7. Bone and Mineral Unit, Oregon Health and Science University, Portland, OR, USA;8. Departments of Family and Preventive Medicine and Internal Medicine, University of California at San Diego, San Diego, CA, USA;9. Division of Epidemiology, University of Minnesota, Minneapolis, MN, USA and Minneapolis Veterans Administration Medical Center, Minneapolis, MN, USA;1. Park Nicollet Osteoporosis Center and Institute for Research and Education, Minneapolis, MN, USA and Division of Health Policy and Management, University of Minnesota, Minneapolis, MN, USA;2. Beth Israel Deaconess Medical Center, Boston, MA, USA;3. Department of Medicine, University of Chicago, Chicago, IL, USA;4. Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA, USA;5. San Francisco Coordinating Center, California Pacific Medical Center, San Francisco, CA, USA;6. Division of Epidemiology and Biostatistics, University of California at San Francisco, San Francisco, CA, USA;7. Bone and Mineral Unit, Oregon Health and Science University, Portland, OR, USA;8. Departments of Family and Preventive Medicine and Internal Medicine, University of California at San Diego, San Diego, CA, USA;9. Division of Epidemiology, University of Minnesota, Minneapolis, MN, USA and Minneapolis Veterans Administration Medical Center, Minneapolis, MN, USA;1. Department of Computer Science and Engineering, Seoul National University of Science and Technology, (SeoulTech) Seoul 01811, Republic of Korea;2. School of Computing Science and Engineering, Vellore Institute of Technology (VIT), Vellore-632014, India;1. Division of Neonatal Medicine, Department of Pediatrics, New York Medical College, Maria Fareri Children''s Hospital, Valhalla, NY;2. Department of Internal Medicine, Pediatrics, and Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, and Health Policy and Management, UCLA Fielding School of Public Health, Los Angeles, CA;3. Division of Pediatric Pulmonology, Department of Pediatrics, University of Wisconsin School of Medicine and Public Health, Madison, WI;4. Department of Pediatrics, Eugene S. Farley, Jr Health Policy Center, University of Colorado School of Medicine, Denver, CO;5. Division of Pediatric Hematology/Oncology, C.S. Mott Children''s Hospital, University of Michigan School of Medicine, Ann Arbor, MI |
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| Abstract: | Iron deficiency impairs vitamin A (VA) metabolism in the rat but the mechanisms involved are unknown and the effect during development has not been investigated. We investigated the effect of pregnancy and maternal iron deficiency on VA metabolism in the mother and fetus. 54 rats were fed either a control or iron deficient diet for 2 weeks prior to mating and throughout pregnancy. Another 15 female rats followed the same diet and were used as non-pregnant controls. Maternal liver, placenta and fetal liver were collected at d21 for total VA, retinol and retinyl ester (RE) measurement and VA metabolic gene expression analysis. Iron deficiency increased maternal hepatic RE (P < .05) and total VA (P < .0001), fetal liver RE (P < .05), and decreased placenta total VA (P < .05). Pregnancy increased Cellular Retinol Binding Protein (CRBP)-II gene expression by 7 fold (P = .001), decreased VA levels (P = .0004) and VA metabolic gene expression (P < .0001) in the liver. Iron deficiency increased hepatic CRBPII expression by a further 2 fold (P = .044) and RBP4 by ~ 20% (P = .005), increased RBPR2 and decreased CRBPII, LRAT, and TTR in fetal liver, while it had no effect on VA metabolic gene expression in the placenta. Hepatic CRBPII expression is increased by pregnancy and further increased by iron deficiency, which may play an important role in VA metabolism and homeostasis. Maternal iron deficiency also alters VA metabolism in the fetus, which is likely to have consequences for development. |
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