HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Schneider, L. Articles by Torresani, J. Search for Related Content PubMed PubMed Citation Articles by Schneider, L. Articles by Torresani, J.

¹ INSERM U476 and IFR 35, Université de la Méditerranée, Faculté de Medecine, 13385 Marseille, Cedex 5, France
² Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA

(Requests for offprints should be addressed to J Torresani; Email: Janine.Torresani{at}medecine.univ-mrs.fr)

1,25-(OH)₂-Vitamin D3 (1,25-D3) and the thyroid hormone tri-iodothyronine (T₃) were previously shown to behave as adipogenic agents in murine Ob17 preadipocytes. Moreover, these agents interfere with each other’s action during adipocyte differentiation. T₃ receptor (TR) expression and a downmodulation of T₃ binding sites (TR sites) by 1,25-D3 were also reported. A cross talk at the T₃ and 1,25-D3 receptor (VDR) level was suggested. We report here that Ob17 cells contain VDR receptor sites in markedly modulated number. This includes a sharp decrease during differentiation that was largely counteracted by 1,25-D3 added to preadipocytes in physiological, adipogenic concentrations. In parallel, the VDR mRNA level did not change significantly, neither did a variant produced by alternative splicing in the penultimate exon and defined for the first time in the mouse. The differentiation- and 1,25-D3-related modulations of VDR sites are likely to be, at least for the most part, the result of variations in abundance of the VDR protein, and may thus mainly involve post-translational events. In contrast, the addition of T₃ to the preadipocytes amplified the differentiation-related decrease in VDR sites, even in the presence of 1,25-D3. T₃ significantly decreased the levels of VDR transcripts and thus mainly exerts a pretranslational action. With regard to the reciprocal downmodulation of the TR sites (identified as almost exclusively of the TR type) by physiological concentrations of 1,25-D3, a post-translational action and a sequestration of the TR sites had previously been suggested and are further studied here. Analyses of receptor properties after co-incubations of recombinant VDRs and TRs did not favour direct VDR–TR interaction as a main cause of TR site sequestration. Interestingly, when taken together, the data on downregulation of VDRs and TRs by the alternate ligands define a potential step in the cross talk exerted between 1,25-D3 and T₃ for their adipogenic action. In addition, the present results also show for the first time that 1,25-D3 acts as a strong trigger of a transient expression of TRß1 subtype at an early preadipocyte step, an effect that had previously been assigned to T₃. This last interesting event introduces further incentive for deciphering the T₃/1,25-D3 cross talk in preadipocyte differentiation.