**3. Conclusion**

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 resistance in obesity remains an open question.
