**Abstract**

Obesity, being an epidemy these days, is the trigger of metabolic disturbances such as cardiovascular disease, type 2 diabetes, and insulin resistance. Defined as an increase in fat storage, adipose tissue has been put under the spotlight as the culprit of these conditions, as it is composed not only by adipocytes but of any immune system cell and a singular extracellular matrix. Its behavior under acute and chronic hypercaloric states is quite different; persistent hypertrophy in the latter creates hypoxia, resulting in the release of reactive oxygen species and proinflammatory cytokines that impact on the immune response type of the resident leucocytes, mainly macrophages. Hypertrophy over hyperplasia, adipose tissue macrophages-M1 phenotype polarization, and the adipokines/myokines profile are thought to be regulated by foreign microRNAs, delivered from surrounding or distant cells by exosomes through the bloodstream. In this chapter, we focus on adipose tissue immunometabolism and how obesity causes the chronic inflammatory state, and, subsequently, this stablishes a pathologic adiposity*,* characterized by dyslipidemia and insulin resistance (IR).

**Keywords:** obesity, adipose tissue, adipose tissue macrophages-M1 phenotype, exosomes, microRNAs, insulin resistance, pathologic adiposity

## **1. Introduction**

Novel findings on the immune-regulatory processes and metabolic mechanisms may open new avenues in the complex diseases as well as obesity; research on basic and clinical advances in immunometabolism has evolved rapidly during the past years, and the emergence of new tools for the detection and characterization of regulation of inflammation in systemic inflammatory diseases with metabolic comorbidity may play an imperative role.

Interplay in regulation of inflammation and metabolic risk factors are a complex cluster. The inflammatory condition associated with adipose tissue represents a triggering factor in the etiology of the obesity pathological-mechanism and mainly contributes to the related disease outcomes.

The purpose of this chapter is to address recent findings in metabolic, molecular biology, function, and pathology of the immune response to inflammation on the

role of the immunometabolism in obesity. That containing significant new findings in the field, presenting the state of the art findings, will offer the new insights into interplay in the regulation of inflammation, especially in the tools of the comorbidity, in order to know their mechanisms by metabolic and immune response that cause disease.
