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Yaacov Frishberg - One of the best experts on this subject based on the ideXlab platform.
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VitAmin A Deficiency AssociAted with urinAry retinol binding protein wAsting in Dent’s diseAse
Pediatric Nephrology, 2012Co-Authors: Rachel Becker-cohen, Choni Rinat, Efrat Ben-shalom, Sofia Feinstein, Heftziba Ivgi, Yaacov FrishbergAbstract:BAckground Three pAtients with Dent’s diseAse presented with complAints of impAired night vision or xerophthAlmiA And were found to hAve severely decreAsed serum retinol concentrAtions. Retinol, bound to its cArrier retinol-binding protein (RBP), is filtered At the glomerulus And reAbsorbed At the proximAl tubule. We hypothesized thAt urinAry loss of retinol-RBP complex is responsible for decreAsed serum retinol. Objective And methods The study Aim wAs to investigAte VitAmin A stAtus And RBP in serum And urine of pAtients with geneticAlly confirmed Dent’s diseAse. Results Eight pAtients were studied, three boys hAd clinicAl VitAmin A Deficiency, three hAd AsymptomAtic Deficiency, And two young men with Dent’s diseAse And impAired renAl function hAd normAl retinol vAlues. Serum RBP concentrAtions were low in pAtients with VitAmin A Deficiency And were correlAted with VitAmin A levels. UrinAry RBP concentrAtions were increAsed in All pAtients (2,000-fold), regArdless of VitAmin A stAtus. This wAs in contrAst to pAtients with glomerulAr proteinuriA who hAd only mildly increAsed urinAry RBP with normAl serum RBP And VitAmin A, And pAtients with cystinosis with impAired renAl function who hAd mAssive urinAry RBP losses but without A decreAse in serum RBP or VitAmin A levels. TreAtment with VitAmin A supplements in pAtients with retinol Deficiency resulted in rApid resolution of oculAr symptoms And An increAse in serum retinol concentrAtions. Conclusions VitAmin A Deficiency is common in pAtients with Dent's diseAse And preserved renAl function. We therefore recommend screening these pAtients for retinol Deficiency And treAting them before visuAl symptoms develop.
Véronique Pallet - One of the best experts on this subject based on the ideXlab platform.
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VitAmin A Deficiency impAirs contextuAl feAr memory in rAts: AbnormAlities in the glucocorticoid pAthwAy
Journal of Neuroendocrinology, 2019Co-Authors: Damien Bonhomme, Serge Alfos, Véronique Pallet, Scott P. Webster, Mathieu Wolff, Katia TouyarotAbstract:VitAmin A And its Active metAbolite, retinoic Acid (RA), plAy A key role in the mAintenAnce of cognitive functions in the Adult brAin. Depletion of RA using the VitAmin A Deficiency (VAD) model in WistAr rAts leAds to spAtiAl memory deficits in relAtion to elevAted intrAhippocAmpAl bAsAl corticosterone (CORT) levels And increAsed hippocAmpAl 11β-hydroxysteroid dehydrogenAse type 1 (11β-HSD1) Activity. All of these effects Are normAlised by VitAmin A supplementAtion. However, it is unknown whether VitAmin A stAtus Also modulAtes contextuAl feAr conditioning (CFC) in A glucocorticoid-AssociAted feAr memory tAsk dependent on the functionAl integrity of the hippocAmpus. In the present study, we investigAted the impAct of VAD And VitAmin A supplementAtion in Adult mAle rAts on feAr memory processing, plAsmA CORT levels, hippocAmpAl retinoid receptors And 11β-HSD1 expression following A novelty-induced stress. We Also exAmined whether VitAmin A supplementAtion or A single injection of UE2316, A selective 11β-HSD1 inhibitor, known to modulAte locAl glucocorticoid levels, hAd Any beneficiAl effects on contextuAl feAr memory And biochemicAl pArAmeters in VAD rAts. We provide evidence thAt VAD rAts exhibit A decreAsed feAr conditioning response during trAining with A poor contextuAl feAr memory 24 hours lAter. These VAD-induced cognitive impAirments Are AssociAted with elevAted plAsmA CORT levels under bAsAl conditions, As well As following A stressful event, with sAturAted CORT releAse, Altered hippocAmpAl retinoid receptors And 11β-HSD1 expression. VitAmin A supplementAtion normAlises VAD-induced feAr conditioning trAining deficits And All biochemicAl effects, Although it cAnnot prevent feAr memory deficits. Moreover, A single injection of UE2316 not only impAirs contextuAl feAr memory, but Also reduces plAsmA CORT levels, regArdless of the VitAmin A stAtus And decreAses slightly hippocAmpAl 11β-HSD1 Activity in VAD rAts following stress. The present study highlights the importAnce of VitAmin A stAtus with respect to modulAting feAr memory conditioning in relAtion to plAsmA CORT levels And hippocAmpAl 11β-HSD1.
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VitAmin A Deficiency And relAtionAl memory deficit in Adult mice: relAtionships with chAnges in brAin retinoid signAlling
Behavioural Brain Research, 2003Co-Authors: Nicole Etchamendy, Valérie Enderlin, Paul Higueret, Véronique Pallet, Aline Marighetto, Robert JaffardAbstract:VitAmin A And its derivAtives, the retinoids, hAve recently been reported to be implicAted in the synAptic plAsticity of the hippocAmpus And in cognitive functions. Acting viA trAnscription fActors, retinoids cAn regulAte gene expression viA their nucleAr receptors [retinoic Acid receptors (RARs) And retinoid X receptors (RXRs)]. We recently showed thAt A moderAte (About 30%) hypoexpression of brAin (And hippocAmpAl) retinoid signAlling, like thAt nAturAlly occurring in the Aged brAin of mice, might be relAted to A selective relAtionAl memory deficit. To further Assess this hypothesis, the present study investigAted the effects of VitAmin A deprivAtion of vArying durAtion both on the brAin expression of retinoid receptors (RARbetA And RXRbetA/gAmmA) And two AssociAted tArget genes [tissue-type trAnsglutAminAse (tTG) And neurogrAnin, (RC3)], And on rAdiAl mAze discriminAtion leArning using young Adult mice As subjects. We observed thAt irrespective of its durAtion (i.e. 31 or 39 weeks), VitAmin A deprivAtion resulted in A significAnt reduction (25-30%) in the expression of brAin RARbetA, RXRbetA/gAmmA And tTG mRNAs. Conversely, only the 39-week condition wAs found to induce A significAnt decreAse in brAin RC3 mRNAs contents And A selective relAtionAl memory impAirment. FinAlly, dAily AdministrAtion of retinoic Acid (RA) fAiled to reverse the 39-week VitAmin A Deficiency (VAD)-relAted cognitive deficit And to fully normAlise the AssociAted brAin retinoid hyposignAlling. In pArticulAr, there wAs no evidence for An up-regulAting effect of RA on whole brAin (And hippocAmpAl) RC3 mRNAs of the 39-week-depleted mice. The results show thAt post-nAtAl VAD mAy induce A selective memory impAirment And give further support to the hypothesis thAt the fine regulAtion of retinoid-mediAted gene expression is importAnt for optimAl brAin functioning And higher cognition.
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Triiodothyronine AdministrAtion reverses VitAmin A Deficiency-relAted hypo-expression of retinoic Acid And triiodothyronine nucleAr receptors And of neurogrAnin in rAt brAin
British Journal of Nutrition, 2003Co-Authors: Marianne Husson, Valérie Enderlin, Serge Alfos, Paul Higueret, Catherine Feart, Véronique PalletAbstract:Recent studies hAve reveAled thAt retinoids plAy An importAnt role in the Adult centrAl nervous system And cognitive functions. Previous investigAtions in mice hAve shown thAt VitAmin A Deficiency (VAD) generAtes A hypo-expression of retinoic Acid (RA, the Active metAbolite of VitAmin A) receptors And of neurogrAnin (RC3, A neuronAl protein involved in synAptic plAsticity) And A concomitAnt selective behAviourAl impAirment. Knowing thAt RC3 is both A triiodothyronine (T3) And A RA tArget gene, And in considerAtion of the relAtionships between the signAlling pAthwAys of retinoids And thyroid hormones, the involvement of T3 on RA signAlling functionAlity in VAD wAs investigAted. Thus, the effects of VitAmin A depletion And subsequent AdministrAtion with RA And/or T3 on the expression of RA nucleAr receptors (RAR, RXR), T3 nucleAr receptor (TR) And on RC3 in the brAin were exAmined. RAts fed A VitAmin A-deficient diet for 10 weeks exhibited A decreAsed expression of RAR, RXR And TR mRNA And of RC3 mRNA And proteins. RA AdministrAtion to these VitAmin A-deficient rAts reversed only the RA hypo-signAlling in the brAin. Interestingly, T3 is Able to restore its own brAin signAlling simultAneously with thAt of VitAmin A And the hypo-expression of RC3. These results obtAined in vivo reveAled thAt one of the consequences of VAD is A dysfunction in the thyroid signAlling pAthwAy in the brAin. This seems of cruciAl importAnce since the down regulAtion of RC3 observed in the depleted rAts wAs corrected only by T3.
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VitAmin A Deficiency DecreAses the Expression of RARβ And RXRβ/γ in Adult Mouse BrAin: Effect of RA AdministrAtion
Nutritional Neuroscience, 2000Co-Authors: Valérie Enderlin, Denise Higueret, Serge Alfos, Marianne Husson, Robert Jaffard, Paul Higueret, Véronique PalletAbstract:Recent studies hAve reveAled A novel And unexpected role of VitAmin A, viA its nucleAr receptors, in higher cognitive functions. We exAmined, in mouse brAin, the impAct of VitAmin A stAtus on the level of retinoic Acid nucleAr receptor (RAR And RXR) expression And on one of their responsive genes, thAt of the tissue trAnsglutAminAse (tTG). WeAnling mAle C57B1/6 mice fed A VitAmin A deficient diet developed A VitAmin A Deficiency which wAs chArActerized, After 26 weeks, by the depletion of serum retinol, liver retinol And retinyl pAlmitAte, And by the decreAsed Activity of liver tTG. After 27 weeks of the diet, the VitAmin A depleted mice exhibited A significAntly lower Amount of brAin RAR β And RXR β/γ mRNA relAtive to control mice. VitAmin A Deficiency Also resulted in A reduced expression of tTG. When 35-week depleted mice were subsequently AdministrAted RA for 28 dAys, the expression of RA nucleAr receptors And tTG wAs significAntly induced. The VitAmin A Deficiency mouse model And repletion provides A physiologicAl system for monitoring the effects of VitAmin A stAtus on gene expression And on neurobiologicAl processes in the Adult brAin.
Rachel Becker-cohen - One of the best experts on this subject based on the ideXlab platform.
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VitAmin A Deficiency AssociAted with urinAry retinol binding protein wAsting in Dent’s diseAse
Pediatric Nephrology, 2012Co-Authors: Rachel Becker-cohen, Choni Rinat, Efrat Ben-shalom, Sofia Feinstein, Heftziba Ivgi, Yaacov FrishbergAbstract:BAckground Three pAtients with Dent’s diseAse presented with complAints of impAired night vision or xerophthAlmiA And were found to hAve severely decreAsed serum retinol concentrAtions. Retinol, bound to its cArrier retinol-binding protein (RBP), is filtered At the glomerulus And reAbsorbed At the proximAl tubule. We hypothesized thAt urinAry loss of retinol-RBP complex is responsible for decreAsed serum retinol. Objective And methods The study Aim wAs to investigAte VitAmin A stAtus And RBP in serum And urine of pAtients with geneticAlly confirmed Dent’s diseAse. Results Eight pAtients were studied, three boys hAd clinicAl VitAmin A Deficiency, three hAd AsymptomAtic Deficiency, And two young men with Dent’s diseAse And impAired renAl function hAd normAl retinol vAlues. Serum RBP concentrAtions were low in pAtients with VitAmin A Deficiency And were correlAted with VitAmin A levels. UrinAry RBP concentrAtions were increAsed in All pAtients (2,000-fold), regArdless of VitAmin A stAtus. This wAs in contrAst to pAtients with glomerulAr proteinuriA who hAd only mildly increAsed urinAry RBP with normAl serum RBP And VitAmin A, And pAtients with cystinosis with impAired renAl function who hAd mAssive urinAry RBP losses but without A decreAse in serum RBP or VitAmin A levels. TreAtment with VitAmin A supplements in pAtients with retinol Deficiency resulted in rApid resolution of oculAr symptoms And An increAse in serum retinol concentrAtions. Conclusions VitAmin A Deficiency is common in pAtients with Dent's diseAse And preserved renAl function. We therefore recommend screening these pAtients for retinol Deficiency And treAting them before visuAl symptoms develop.
Ane Baerent Fisker - One of the best experts on this subject based on the ideXlab platform.
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An enigmA why VitAmin A supplementAtion does not AlwAys reduce mortAlity even though VitAmin A Deficiency is AssociAted with increAsed mortAlity
International Journal of Epidemiology, 2015Co-Authors: Christine Stabell Benn, Peter Aaby, Rob J W Arts, Kristoffer Jarlov Jensen, Mihai G Netea, Ane Baerent FiskerAbstract:BAckground: VitAmin A Deficiency (VAD) is AssociAted with increAsed mortAlity. To prevent VAD, WHO recommends high-dose VitAmin A supplementAtion (VAS) every 4‐6 months for children Aged between 6 months And 5 yeArs of Age in countries At risk of VAD. The policy is bAsed on rAndomized clinicAl triAls (RCTs) conducted in the lAte 1980s And eArly 1990s. Recent RCTs indicAte thAt the policy mAy hAve ceAsed to be beneficiAl. In Addition, RCTs Attempting to extend the benefits to younger children hAve yielded conflicting results. StrAtified AnAlyses suggest thAt whereAs some subgroups benefit more thAn expected from VAS, other subgroups mAy experience negAtive effects. Methods And Results: We reviewed the potentiAl modifiers of the effect of VAS. The vAriAble effect of VAS wAs not explAined by underlying differences in VAD. RAther, the effect mAy depend on the sex of the child, the vAccine stAtus And previous supplementAtion with VitAmin A. VitAmin A is known to Affect the Th1/Th2 bAlAnce And, in Addition, recent evidence suggests thAt VitAmin A mAy Also induce epigenetic chAnges leAding to downregulAtion of the innAte immune response. Thus VAS protects AgAinst VAD but hAs Also importAnt And long-lAsting immunologicAl effects, And the effect of providing VAS mAy vAry depending on the stAte of the immune system. Conclusions: To design optimAl VAS progrAmmes which tArget those who benefit And Avoid those hArmed, more studies Are needed. Work is ongoing to define whether neonAtAl VAS should be considered in subgroups. In the most recent RCT in older children, VAS doubled the mortAlity for mAles but hAlved mortAlity for femAles. Hence, we urgently need to re-Assess the effect of VAS on older children in lArge-scAle RCTs powered
Heftziba Ivgi - One of the best experts on this subject based on the ideXlab platform.
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VitAmin A Deficiency AssociAted with urinAry retinol binding protein wAsting in Dent’s diseAse
Pediatric Nephrology, 2012Co-Authors: Rachel Becker-cohen, Choni Rinat, Efrat Ben-shalom, Sofia Feinstein, Heftziba Ivgi, Yaacov FrishbergAbstract:BAckground Three pAtients with Dent’s diseAse presented with complAints of impAired night vision or xerophthAlmiA And were found to hAve severely decreAsed serum retinol concentrAtions. Retinol, bound to its cArrier retinol-binding protein (RBP), is filtered At the glomerulus And reAbsorbed At the proximAl tubule. We hypothesized thAt urinAry loss of retinol-RBP complex is responsible for decreAsed serum retinol. Objective And methods The study Aim wAs to investigAte VitAmin A stAtus And RBP in serum And urine of pAtients with geneticAlly confirmed Dent’s diseAse. Results Eight pAtients were studied, three boys hAd clinicAl VitAmin A Deficiency, three hAd AsymptomAtic Deficiency, And two young men with Dent’s diseAse And impAired renAl function hAd normAl retinol vAlues. Serum RBP concentrAtions were low in pAtients with VitAmin A Deficiency And were correlAted with VitAmin A levels. UrinAry RBP concentrAtions were increAsed in All pAtients (2,000-fold), regArdless of VitAmin A stAtus. This wAs in contrAst to pAtients with glomerulAr proteinuriA who hAd only mildly increAsed urinAry RBP with normAl serum RBP And VitAmin A, And pAtients with cystinosis with impAired renAl function who hAd mAssive urinAry RBP losses but without A decreAse in serum RBP or VitAmin A levels. TreAtment with VitAmin A supplements in pAtients with retinol Deficiency resulted in rApid resolution of oculAr symptoms And An increAse in serum retinol concentrAtions. Conclusions VitAmin A Deficiency is common in pAtients with Dent's diseAse And preserved renAl function. We therefore recommend screening these pAtients for retinol Deficiency And treAting them before visuAl symptoms develop.
