**1. Introduction**

Inmmunometabolism has been defined as the interphase between metabolism and immune response [1, 2], in which, adipose tissue plays a key role. Leptin was the first molecule described linking the immune system with metabolism. The first leptin function described was appetite control; however, nowadays it has been described with multiple permissive functions, like immune homeostasis, among others (**Figure 1**) [3]. On innate and adaptive immune response cells, leptin can mainly increase cytokine expression, cell surface adhesion molecules and chemokine receptors [3, 4]. Additional to leptin, free fatty acid receptors family (FFARs) has been reported to be expressed on key cell types regulating both: energy homoeostasis and inflammatory responses [2]. Obesity induces changes in gut microbiota, it has been reported that *Bacteroidetes* and *Firmicutes* phyla produce high levels of the short chain free fatty acids (SCFAs) C2–C4 which are the main agonists for FFAR2 [5]; at the same time, microbiota can influence innate and adaptive immune responses [6, 7]. These examples make clear the interrelation between metabolism and the immune system. We will focus along this chapter in alterations of this interphase due to the presence of obesity.

**Figure 1.** Neuroendocrine immune system.
