Vitamin A Deficiency Decreases the Expression of RARβ and RXRβ/γ in Adult Mouse Brain: Effect of RA Administration
V Enderlin1, D Higueret2, S Alfos1
1a Laboratoire de Nutrition et Signalisation Cellulaire , ISTAB , Avenue des Facultés , Université Bordeaux I , 33405 Talence, France.
Nutritional Neuroscience
|July 15, 2016
Summary
Vitamin A deficiency impacts brain gene expression, reducing retinoic acid receptors (RAR and RXR) and tissue transglutaminase (tTG). Supplementation restored these levels, highlighting vitamin A
Area of Science:
- Neuroscience
- Molecular Biology
- Nutritional Science
Background:
- Emerging evidence suggests vitamin A influences higher cognitive functions.
- Nuclear receptors, including retinoic acid receptors (RAR and RXR), mediate vitamin A's actions.
- Tissue transglutaminase (tTG) is a gene responsive to these receptors.
Purpose of the Study:
- To investigate the effect of vitamin A deficiency on RAR, RXR, and tTG expression in the adult mouse brain.
- To establish a mouse model for studying vitamin A's neurobiological roles.
Main Methods:
- Induction of vitamin A deficiency in weanling male C57B1/6 mice over 26 weeks.
- Quantification of serum and liver retinol, liver tTG activity, and brain RAR/RXR mRNA levels.
- Administration of retinoic acid (RA) to deficient mice to assess repletion effects.
Main Results:
- Vitamin A deficiency led to decreased serum retinol, liver retinol, liver tTG activity, and brain RAR β and RXR β/γ mRNA.
- Reduced expression of tTG was observed in vitamin A-deficient mice.
- Retinoic acid administration significantly increased the expression of RA nuclear receptors and tTG.
Conclusions:
- Vitamin A status critically affects the expression of its nuclear receptors and target genes like tTG in the adult brain.
- The developed mouse model is suitable for studying the neurobiological impact of vitamin A.
- This research underscores vitamin A's importance in brain function and gene regulation.
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