Triiodothyronine administration reverses vitamin A deficiency-related hypo-expression of retinoic acid and triiodothyronine nuclear receptors and of neurogranin in rat brain
| Autor: | Paul Higueret, Catherine Féart, Véronique Pallet, Serge Alfos, Marianne Husson, V Enderlin |
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| Rok vydání: | 2003 |
| Předmět: |
Male
Vitamin Retinyl Esters medicine.medical_specialty Receptors Retinoic Acid medicine.drug_class Blotting Western Retinoic acid Medicine (miscellaneous) Nerve Tissue Proteins Tretinoin Biology Retinoid X receptor chemistry.chemical_compound GTP-Binding Proteins Internal medicine medicine Animals Protein Glutamine gamma Glutamyltransferase 2 RNA Messenger Neurogranin Retinoid Rats Wistar Vitamin A Brain Chemistry Receptors Thyroid Hormone Transglutaminases Nutrition and Dietetics Triiodothyronine Reverse Transcriptase Polymerase Chain Reaction Vitamin A Deficiency Retinol medicine.disease Rats Vitamin A deficiency Retinoid X Receptors Endocrinology Liver chemistry Calmodulin-Binding Proteins Diterpenes Transcription Factors |
| Zdroj: | British Journal of Nutrition. 90:191-198 |
| ISSN: | 1475-2662 0007-1145 |
| Popis: | 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 T3on RA signalling functionality in VAD was investigated. Thus, the effects of vitamin A depletion and subsequent administration with RA and/or T3on the expression of RA nuclear receptors (RAR, RXR), T3nuclear 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, T3is 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. |
| Databáze: | OpenAIRE |
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