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2 expression in adipocytes
1 Department of Animal Sciences, Comparative Medicine Center, Purdue University, West Lafayette, Indiana, USA
* To whom correspondence should be addressed. E-mail: spurloc0{at}purdue.edu.
Circulating adiponectin concentrations are lower in association with obesity and insulin resistance, both of which are physiological conditions frequently accompanied by chronic increases in circulating interleukin-6 (IL-6) and(or) tumor necrosis factor-
(TNF). Adiponectin suppresses activation of the nuclear factor kappa B (NFkB) transcription factor in aortic endothelial cells and porcine macrophages. We hypothesized that adiponectin acts as an anti-inflammatory hormone and suppresses the activation of NFkB, which culminates in increased cytokine production by adipocytes and other immune cells. Because PPAR
2 exerts anti-inflammatory actions and antagonizes the transcriptional activity of NFkB, we also determined if adiponectin alters PPAR2 expression in pig adipocytes. Additionally, we determined whether interferon- (IFN) altered the expression of PPAR2 adiponectin in the presence or absence of adiponectin. Primary pig adipocytes were recovered from subcutaneous adipose tissue, and incubated in the presence and absence of lipopolysaccharide (LPS, 10 µg/mL) and adiponectin (30 µg/mL), and nuclear extracts recovered for electrophoretic mobility shift assays to assess nuclear localization of NFkB. Whereas LPS caused a marked increase in nuclear NFkB, adiponectin attenuated the response, and also attenuated the induction of IL-6 expression by LPS (P < 0.05). We extended this work to 3T3-L1 adipocytes, and obtained similar results. Additionally, adiponectin antagonized the endotoxin-induced increase in TNF mRNA expression (P < 0.05) and tended (P < 0.065) to diminish the accumulation of this cytokine in the culture media in 3T3-L1 adipocytes. Incubation with adiponectin (30 µg/mL) resulted in a marked upregulation of PPAR2 mRNA (P < 0.05) within 5 hours. Although IFN did not reduce the basal expression of PPAR2, it did suppress the induction of this PPAR by adiponectin (P < 0.05). These data indicate that adiponectin is a local regulator of inflammation in the adipocyte and adipose tissue, and that the mechanism includes regulation of the NFkB transcription factor, and possibly an induction of PPAR2.
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