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Induction of STEAP 4 correlates with 1,25‐dihydroxyvitamin D 3 stimulation of adipogenesis in mesenchymal progenitor cells derived from human adipose tissue
Author(s) -
Narvaez C. J.,
Simmons K. M.,
Brunton J.,
Salinero A.,
Chittur S. V.,
Welsh J. E.
Publication year - 2013
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.24371
Subject(s) - adipogenesis , mesenchymal stem cell , adipose tissue , stimulation , progenitor cell , microbiology and biotechnology , progenitor , endocrinology , biology , chemistry , medicine , stem cell
ABSTRACT The vitamin D receptor (VDR) is expressed in human adipocytes and is transiently induced during early adipogenesis in mesenchymal progenitor cell models. VDR null mice exhibit enhanced energy expenditure and reduced adiposity even when fed high fat diets. Adipocyte‐specific transgenic‐expression of human VDR in mice enhances adipose tissue mass, indicating that VDR activation in adipocytes enhances lipid storage in vivo. In these studies, we conducted genomic profiling and differentiation assays in primary cultures of human adipose‐derived mesenchymal progenitor cells to define the role of the VDR and its ligand 1,25‐dihydroxyvitamin D 3 (1,25D) in adipogenesis. In the presence of adipogenic media, 1,25D promoted lipid accumulation and enhanced the expression of FABP4, FASN, and PPARγ. Mesenchymal cells derived from 6‐month old VDR null mice exhibited impaired adipogenesis ex vivo but differentiation was restored by stable expression of human VDR. STEAP4, a gene that encodes a metalloreductase linked to obesity, insulin sensitivity, metabolic homeostasis and inflammation, was highly induced in human adipose cells differentiated in the presence of 1,25D but was minimally affected by 1,25D in undifferentiated precursors. These studies provide a molecular basis for recent epidemiological associations between vitamin D status, body weight and insulin resistance which may have relevance for prevention or treatment of metabolic syndrome and obesity. J. Cell. Physiol. 228: 2024–2036, 2013. © 2013 Wiley Periodicals, Inc.