title: Vitamin A supplementation redirects the flow of retinyl esters from peripheral to central organs of neonatal rats raised under vitamin A-marginal conditions.
abstract: Background:Vitamin A (VA; retinol) supplementation is used to reduce child mortality in countries with high rates of malnutrition. Existing research suggests that neonates (<1 mo old) may have a limited capacity to store VA in organs other than the liver; however, knowledge about VA distribution and kinetics in individual, nonhepatic organs is limited.Objective:We examined retinol uptake and turnover in nonhepatic organs, including skin, brain, and adipose tissue, in neonatal rats without and after VA supplementation.Design:Sprague-Dawley neonatal rats (n= 104) were nursed by mothers fed a VA-marginal diet (0.35 mg retinol/kg diet) and treated on postnatal day 4 with an oral dose of either VA (6 μg retinyl palmitate/g body weight) or canola oil (control), both containing 1.8 μCi of [3H]retinol. Subsequently, pups (n= 4 · group-1· time-1) were killed at 13 different times from 30 min to 24 d after dosing. The fractional and absolute transfer of chylomicron retinyl esters (CM-REs), retinol bound to retinol-binding protein (RBP-ROH), and total retinol were estimated in WinSAAM software.Results:VA supplementation redirected the flow of CM-REs from peripheral to central organs and accumulated mainly in the liver. The RBP-ROH released from the liver was acquired mainly by the peripheral tissues but not retained efficiently, causing repeated recycling of retinol between plasma and tissues (541 compared with 5 times in the supplemented group and control group, respectively) and its rapid turnover in all organs, except the brain and white adipose tissue. Retinol stores in the liver lasted for ∼2 wk before being gradually transferred to other organs.Conclusions:VA supplementation administered in a single high dose during the first month after birth is readily acquired but not retained efficiently in peripheral tissues of neonatal rats, suggesting that a more frequent, lower-dose supplementation may be necessary to maintain steady VA concentrations in rapidly developing neonatal tissues.
authors.affiliation: Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA.
authors.forename: Joanna K
authors.identifier: 0000-0002-9187-9473
authors.initials: JK
authors.lastname: Hodges
authors.affiliation: Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA.
authors.forename: Libo
authors.initials: L
authors.lastname: Tan
authors.affiliation: Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA.
authors.forename: Michael H
authors.initials: MH
authors.lastname: Green
authors.affiliation: Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA acr6@psu.edu.
authors.forename: A Catharine
authors.initials: AC
authors.lastname: Ross
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D002914:Chylomicrons / Q000378:metabolism; D019587:Dietary Supplements; D004224:Diterpenes; D004305:Dose-Response Relationship, Drug; D004952:Esters / Q000378:metabolism*; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D008099:Liver / Q000378:metabolism*; D008297:Male; D017207:Rats, Sprague-Dawley; D012177:Retinol-Binding Proteins / Q000378:metabolism; D000084562:Retinyl Esters; D012867:Skin / Q000378:metabolism*; D014801:Vitamin A / Q000031:analogs & derivatives / Q000097:blood / Q000378:metabolism / Q000493:pharmacokinetics*; D014802:Vitamin A Deficiency / Q000097:blood / Q000378:metabolism / Q000517:prevention & control
chemical_list: D002914:Chylomicrons; D004224:Diterpenes; D004952:Esters; D012177:Retinol-Binding Proteins; D000084562:Retinyl Esters; D014801:Vitamin A; C014794:retinol palmitate
keywords: chylomicron; extrahepatic; growth and development; mathematical modeling; neonate; retinyl esters; vitamin A deficiency; vitamin A metabolism; vitamin A supplementation