Niacin Increases Chemerin mRNA Abundance in Differentiated Bovine Preadipocytes In Vitro

Monday, July 21, 2014
Exhibit Hall AB (Kansas City Convention Center)
Christina Kopp , Institute of Animal Science, Physiology & Hygiene Unit, University of Bonn, Bonn, Germany
Hamed Khalilvandi-Behroozyar , Department of Animal Science, Urmia University, Urmia, Iran
Helga Sauerwein , University of Bonn, Institute of Animal Science, Bonn, Germany
Manfred Mielenz , Leibniz Institute for Farm Animal Biology (FBN), Institute of Nutritional Physiology, Dummerstorf, Germany
Abstract Text: Chemerin is thought to be involved in controlling immune responses as a chemoattractant for antigen-presenting cells and has anti-inflammatory as well as pro-inflammatory functions; the latter are linked with obesity and insulin resistance. It is highly expressed as prochemerin in liver and adipose tissue and was recently identified as adipokine that regulates adipogenesis and adipocyte metabolism. The role of chemerin on glucose metabolism is controversially discussed. However, chemerin enhances insulin-stimulated glucose uptake, insulin signaling and increases insulin sensitivity in murine adipocytes. Niacin (NA) is an antilipolytic and lipid-lowering compound which is used since decades to treat dyslipidemia in humans. Furthermore, NA affects the secretion of several adipokines (e.g. adiponectin) and improves insulin sensitivity in humans. These effects are mediated through binding the G-protein coupled receptor 109A (GPR109A). Our objective was thus to examine both, the effect of NA on chemerin mRNA expression in bovine adipocytes and the involvement of GPR109A in NA sensing.  A primary cell culture system using differentiated bovine preadipocytes was established. Subcutaneous adipose tissue was collected from 5 Holstein-Friesian cows. Stromal-vascular cells were isolated, pooled and seeded at 2500 cells/cm2. Preadipocytes after 12 d of differentiation were used. After serum starvation (4 h), cells were incubated either with 100 ng/mL pertussis toxin (PTX), a non-selective G-protein uncoupling agent, or PBS for 16 h to characterize the NA mediating pathway. Cells were then treated with NA (10 or 15 µM) for 12 or 24 h or with PBS as controls, respectively. Chemerin mRNA abundance was quantified by qPCR. Data normalization was based on 5 stable reference genes. Statistical analyses were performed using ANOVA with Bonferroni post hoc tests (P<0.05). The mRNA abundance of chemerin was increased 3.3 fold compared to controls after treatment with 10 µM NA for 24 h (P=0.006). Treatment for 12 h or with 15 µM NA showed no difference in the mRNA abundance of chemerin. Pre-incubation with PTX abolished the observed NA-induced increase of chemerin mRNA abundance. Our results showed a NA-stimulated increase of chemerin mRNA expression in differentiated bovine adipocytes, which may point to improved insulin sensitivity by NA. Due to the annihilated increase after PTX treatment, we suggest that GPR109A mediates the effect of NA.

Keywords: chemerin, niacin, bovine adipocytes