Visfatin is regulated by interleukin-6 and affected by the PPAR-γ pathway in BeWo cells

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Abstract

Visfatin, an adipocytokine and cytosolic enzyme with nicotinamide phosphoribosyltransferase (Nampt) activity, is involved in the pathogenesis of numerous metabolic disorders. In addition, the nuclear receptor peroxisome proliferator-activated receptor-γ (PPAR-γ) serves important roles in anti-inflammatory reactions and regulates glucose and lipid metabolism. The aim of the present study was to investigate the effect of interleukin-6 (IL-6) on the expression and secretion of visfatin in BeWo cells, and to determine whether the PPAR-γ pathway is involved in the regulation of visfatin by IL-6. Therefore, BeWo cells were stimulated with serial concentrations of IL-6 or pioglitazone, and the expression levels of visfatin and PPAR-γ were determined by reverse transcription-quantitative polymerase chain reaction and western blotting. The results of the present study demonstrated that IL-6 downregulated the mRNA levels of visfatin and PPAR-γ, which were strongly associated. Activation of PPAR-γ by pioglitazone resulted in significantly increased expression of visfatin, which abrogated the inhibitory effect of IL-6 on visfatin in BeWo cells. Furthermore, treatment using pioglitazone alone increased the expression and secretion of the visfatin protein, compared with the control or IL-6 alone group. In summary, the findings of the present study suggested that IL-6 inhibited the expression of visfatin and PPAR-γ at the transcriptional level; in addition, activation of PPAR-γ upregulated visfatin at the mRNA and protein expression levels. Therefore, the PPAR-γ signaling pathway may be involved in the regulation of visfatin by IL-6 in BeWo cells. These results may provide novel insight into the roles of visfatin in trophoblastic cells. Furthermore, thiazolidinedione pioglitazone, by upregulating visfatin expression, may promote the energy metabolism of trophoblastic cells, maintain the function of the placenta and improve the outcome of pregnancy.

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Visfatin, an adipocytokine with proinflammatory and immunomodulating properties.

Alexander R Moschen, Arthur Kaser, Barbara Enrich … (2007)

Adipocytokines are mainly adipocyte-derived cytokines regulating metabolism and as such are key regulators of insulin resistance. Some adipocytokines such as adiponectin and leptin affect immune and inflammatory functions. Visfatin (pre-B cell colony-enhancing factor) has recently been identified as a new adipocytokine affecting insulin resistance by binding to the insulin receptor. In this study, we show that recombinant visfatin activates human leukocytes and induces cytokine production. In CD14(+) monocytes, visfatin induces the production of IL-1beta, TNF-alpha, and especially IL-6. Moreover, it increases the surface expression of costimulatory molecules CD54, CD40, and CD80. Visfatin-stimulated monocytes show augmented FITC-dextran uptake and an enhanced capacity to induce alloproliferative responses in human lymphocytes. Visfatin-induced effects involve p38 as well as MEK1 pathways as determined by inhibition with MAPK inhibitors and we observed activation of NF-kappaB. In vivo, visfatin induces circulating IL-6 in BALB/c mice. In patients with inflammatory bowel disease, plasma levels of visfatin are elevated and its mRNA expression is significantly increased in colonic tissue of Crohn's and ulcerative colitis patients compared with healthy controls. Macrophages, dendritic cells, and colonic epithelial cells might be additional sources of visfatin as determined by confocal microscopy. Visfatin can be considered a new proinflammatory adipocytokine.

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NAMPT-Mediated NAD(+) Biosynthesis in Adipocytes Regulates Adipose Tissue Function and Multi-organ Insulin Sensitivity in Mice.

Kelly L. Stromsdorfer, Shintaro Yamaguchi, Myeong Jin Yoon … (2016)

Obesity is associated with adipose tissue dysfunction and multi-organ insulin resistance. However, the mechanisms of such obesity-associated systemic metabolic complications are not clear. Here, we characterized mice with adipocyte-specific deletion of nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting NAD(+) biosynthetic enzyme known to decrease in adipose tissue of obese and aged rodents and people. We found that adipocyte-specific Nampt knockout mice had severe insulin resistance in adipose tissue, liver, and skeletal muscle and adipose tissue dysfunction, manifested by increased plasma free fatty acid concentrations and decreased plasma concentrations of a major insulin-sensitizing adipokine, adiponectin. Loss of Nampt increased phosphorylation of CDK5 and PPARγ (serine-273) and decreased gene expression of obesity-linked phosphorylated PPARγ targets in adipose tissue. These deleterious alterations were normalized by administering rosiglitazone or a key NAD(+) intermediate, nicotinamide mononucleotide (NMN). Collectively, our results provide important mechanistic and therapeutic insights into obesity-associated systemic metabolic derangements, particularly multi-organ insulin resistance.

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Resveratrol supplement inhibited the NF-κB inflammation pathway through activating AMPKα-SIRT1 pathway in mice with fatty liver.

Lingjuan Zhang, Jia Xu, Kai Wang … (2016)

Nonalcoholic fatty liver disease (NAFLD) is characterized by high levels of nonesterified fatty acids (NEFA), inflammation, and hepatic steatosis. Inflammation plays a crucial role in the development of fatty liver. Resveratrol (RSV) supplement could improve inflammatory response and hepatic steatosis, whereas the underlying mechanism was not well understood. In this study, mice fed with high-fat diet (HFD) exhibited severe hepatic injury and high blood concentrations of the inflammatory cytokines TNF-α, IL-6, and IL-1β. Hepatic NF-κB inflammatory pathway was over-induced in HFD mice. In vitro, NEFA treatment further increased NF-κB pathway activation in mice hepatocytes, which then promoted the synthesis of inflammatory cytokines. Interestingly, RSV treatment significantly inhibited overactivation of NF-κB pathway and improved hepatic steatosis. Furthermore, RSV further increased the AMP-activated protein kinaseα (AMPKα) phosphorylation and sirtuin1 (SIRT1) protein levels to inhibit overactivation of NF-κB pathway induced by HFD or high levels of NEFA. AMPKα or SIRT1 inhibition significantly decreased the improvement effect of RSV on the NF-κB pathway induced by high levels of NEFA. Taken together, these findings indicate that RSV supplement decreases the inflammatory level and improves hepatic steatosis through activating AMPKα-SIRT1 pathway. Therefore, these data suggested an important clinical application of RSV in preventing NAFLD in humans.

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Author and article information

Journal

Journal ID (nlm-ta): Mol Med Rep

Journal ID (iso-abbrev): Mol Med Rep

Title: Molecular Medicine Reports

Publisher: D.A. Spandidos

ISSN (Print): 1791-2997

ISSN (Electronic): 1791-3004

Publication date (Print): January 2019

Publication date (Electronic): 20 November 2018

Publication date PMC-release: 20 November 2018

Volume: 19

Issue: 1

Pages: 400-406

Affiliations

[1 ]Department of Obstetrics, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China

[2 ]Department of Obstetrics, Cangzhou People's Hospital, Cangzhou, Hebei 061000, P.R. China

Author notes

Correspondence to: Dr Yan Huo, Department of Obstetrics, Hebei General Hospital, 348 Heping Road, Shijiazhuang, Hebei 050051, P.R. China, E-mail: hy196867@ 123456126.com

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Publisher ID: mmr-19-01-0400

DOI: 10.3892/mmr.2018.9671

PMC ID: 6297763

PubMed ID: 30483779

SO-VID: 4149ffd5-fa77-4516-861e-5771192a386b

License:

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Visfatin is regulated by interleukin-6 and affected by the PPAR-γ pathway in BeWo cells

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Most cited references 38

Visfatin, an adipocytokine with proinflammatory and immunomodulating properties.

NAMPT-Mediated NAD(+) Biosynthesis in Adipocytes Regulates Adipose Tissue Function and Multi-organ Insulin Sensitivity in Mice.

Resveratrol supplement inhibited the NF-κB inflammation pathway through activating AMPKα-SIRT1 pathway in mice with fatty liver.

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