**Author details**

*2.3.8. Macrophage migration inhibitory factor (MIF)*

resistance in obesity remains an open question.

**Acknowledgements**

**3. Conclusion**

142 Glucose Homeostasis

MIF is a multifunctional proinflammatory cytokine which is responsible for inflammatory processes. The primary source and target of MIF have been identified as macrophages [106]. MIF is rapidly released in response to inflammatory stimuli such as lipopolysaccharide, TNFα, and IFN-γ. MIF can have both paracrine and autocrine effects [106-108]. MIF elevates adipose tissue inflammation through amplification of migration, recruitment, and activation of leukocytes at the site of inflammation through upregulation of adhesion molecules such as ICAM-1 and MCP-1 [109-111]. MIF can utilize its chemotactic properties via CXCR2 and CXCR4 in macrophages and T cells, respectively [111]. The interaction of MIF with CXCR4 on the surface of fibroblasts and T cells induced CXCL8 secretion [112]. Interestingly, the alter‐ native MIF receptor CD74, which is traditionally involved in the activation of the mitogenactivated protein kinases pathway, has recently been demonstrated to also mediate macrophage chemotactic responses [113, 114]. Although these roles in macrophage recruit‐ ment have been demonstrated, a recent study showed MIF-/-mice did not exhibit significant

Adipose tissue inflammation and macrophage infiltration are well-established features of obesity. ATMs are separated into at least two groups: M1 and M2. In obesity, more than 90% of recruited monocytes become M1 macrophages that can secrete proinflammatory cytokines resulting in adipose tissue inflammation and insulin resistance. Many studies have identified adipokines that can recruit monocytes into adipose tissue in obesity. Consequently, adipose tissue-derived chemokines may be promising therapeutic targets for insulin resistance and metabolic diseases. Although modulation of a single chemokine can affect the chemotaxis of monocytes when they are studied individually, it is likely that chemokines have overlapping functions in the more complex *in vivo* environment. Moreover, the complicated process of monocyte recruitment and subsequent differentiation into M1 or M2 macrophages in obese adipose tissue appears to be substantially different in mouse and human obesity, which emphasizes the need for investigations in humans. Therefore, whether macrophage depletion stands for an appropriate tool to ameliorate adipose tissue homeostasis and restore insulin

This work was supported by the National Research Foundation of Korea(NRF) grant funded

by the Korea government(MEST) (No. 2013R1A2A1A03010110 and No.2010-0028684).

changes in ATM content compared to WT mice when fed a HFD [115].

Dayea Kim1 , Jong Hyuk Yoon1 , Jaeyoon Kim2 and Sung Ho Ryu1\*

\*Address all correspondence to: sungho@postech.ac.kr

1 Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Gyeongbuk, Republic of Korea

2 The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, Stockholm, Sweden
