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Mediators of Inflammation
Volume 2017, Article ID 1958947, 8 pages
https://doi.org/10.1155/2017/1958947
Research Article

Visfatin Triggers Anorexia and Body Weight Loss through Regulating the Inflammatory Response in the Hypothalamic Microglia

1Division of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 406-772, Republic of Korea
2Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan 682-714, Republic of Korea
3Department of Nano-Bioengineering, Incheon National University, Incheon 406-772, Republic of Korea

Correspondence should be addressed to Jae Geun Kim; rk.ca.uni@mikgj

Received 22 May 2017; Revised 27 August 2017; Accepted 2 November 2017; Published 7 December 2017

Academic Editor: Michal A. Rahat

Copyright © 2017 Thai Hien Tu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Visfatin is an adipokine that is secreted from adipose tissue, and it is involved in a variety of physiological processes. In particular, visfatin has been implicated in metabolic diseases, such as obesity and type 2 diabetes, which are directly linked to systemic inflammation. However, the potential impacts of visfatin on the hypothalamic control of energy homeostasis, which is involved in microglial inflammation, have not fully been investigated. In this study, we found that treatment with exogenous recombinant visfatin protein led to the activation of the inflammatory response in a microglial cell line. In addition, we observed that central administration of visfatin led to the activation of microglia in the hypothalamus. Finally, we found that visfatin reduced food intake and body weight through activating POMC neurons in association with microglia activation in mice. These findings indicate that elevation of central visfatin levels may be associated with homeostatic feeding behavior in response to metabolic shifts, such as increased adiposity following inflammatory processes in the hypothalamus.