Leptin blocks the inhibitory effect of vitamin D on adipogenesis and cell proliferation in 3T3-L1 adipocytes.

Autor: Nobre JL; Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, RJ 20551-030, Brazil., Lisboa PC; Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, RJ 20551-030, Brazil., Carvalho JC; Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, RJ 20551-030, Brazil., Martins MR; Department of Cell Biology, State University of Rio de Janeiro, Rio de Janeiro, RJ 20551-030, Brazil., Vargas S; Department of Cell Biology, State University of Rio de Janeiro, Rio de Janeiro, RJ 20551-030, Brazil., Barja-Fidalgo C; Department of Cell Biology, State University of Rio de Janeiro, Rio de Janeiro, RJ 20551-030, Brazil., de Moura EG; Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, RJ 20551-030, Brazil., de Oliveira E; Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Rio de Janeiro, RJ 20551-030, Brazil. Electronic address: elainedeoliveir@pq.cnpq.br.
Jazyk: angličtina
Zdroj: General and comparative endocrinology [Gen Comp Endocrinol] 2018 Sep 15; Vol. 266, pp. 1-8. Date of Electronic Publication: 2018 Jan 12.
DOI: 10.1016/j.ygcen.2018.01.014
Abstrakt: Recently, we demonstrated high serum leptin and 25(OH)D (calcidiol) in obese animals, with high C/EBP β and PPAR γ expression in adipose tissue. Since the role of vitamin D in adipogenesis remains controversial and hyperleptinemia is found in obesity, we asked if leptin could interfere in vitamin D action on adipocytes. Here, we studied the direct effect of these two hormones upon 3T3L1 preadipocytes incubated with or without 1,25(OH)2D (100 nM, 24 h) and with leptin (10 -7  M, 4 h later). RT-PCR (VDR and Cyp27b1/1α-hydroxylase), western blotting (VDR, Cyp27b1/1α-hydroxylase, ObR-b, C/EBP β , PPAR γ and Bax content), a cell proliferation assay and an Annexin V-FITC binding assay were performed. Incubation with 1,25(OH)2D decreased Cyp27b1/1α-hydroxylase and VDR. Co-incubation of 1,25(OH)2D and leptin did not change Cyp27b1/1α-hydroxylase and had no additive effect upon the decreased VDR mRNA. Incubation with 1,25(OH)2D decreased C/EBP β and PPARγ. In the cell proliferation assay, 1,25(OH)2D decreased the number of 3T3L1 cells. No changes in OBR-b or apoptotic parameters (Bax and annexin-V) were observed. The 1,25(OH)2D decreased pro-adipogenic factors and proliferation of adipocytes. However, since it inhibits the conversion of 25(OH)D to 1,25(OH)2D and VDR mRNA long-term, it could decrease the vitamin D response in adipocytes, leading to greater adipogenesis. The co-incubation of both hormones, simulating what occurs in obesity, even neutralizing the effect on Cyp27b1/1α-hydroxylase, did not change the vitamin D sensitivity but decreased SOCS-3 and pSTAT-3. Thus, an excess of vitamin D and hyperleptinemia could decrease vitamin D sensitivity in adipocytes, contributing to increased adipogenesis.
(Copyright © 2018. Published by Elsevier Inc.)
Databáze: MEDLINE
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