**1. Introduction**

Obesity is defined as an excess amount of body fat that may impair health [1] and has been strongly associated with chronic low-grade or metabolic inflammation characterized by the activation of inflammatory signaling pathways and abnormal secretion of a large set of immune response mediators and several bioactive proteins [2, 3] known as adipokines [4] and a deficit of mediators responsible for the resolution of this process [5]. Within the adipose tissue (AT),

© 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

other cells are also present including preadipocytes, mast cells, and macrophages, which also contribute to this inflammatory environment. Currently and worldwide, obesity is the fifth greatest risk factor for mortality [6], and it is associated with vitamin D deficiency (VDD) [7].

Vitamin D (VD) is essential for the development and maintenance of bone tissue, as well as for normal homeostasis of calcium and phosphorus [8]. Moreover, VD has other major functional roles; it is related to differentiation, cell proliferation, and hormone secretion. It is an important nutrient with crucial role in obesity onset (AT) and in the comorbidities associated with the chronic inflammation [9].

An estimated 80–90% of VD from the human body originates from skin synthesis, with sunlight activation, while the rest is supplied through supplements or food [10]. VD status is measured by means of the plasma levels of 25-hydroxyvitamin D [25(OH)D] or calcidiol, the dominant circulating form and the best indicator of VD status [11]. The action of 1,25(OH)2D, active form of VD [12], is mediated through the vitamin D receptor (VDR), a member of the nuclear receptor superfamily, which regulates the transcription of many target genes [13].

The VDR signaling pathway is crucial for the proper functioning of AT that is called an active endocrine organ, which plays an important role in fat storage and in the production and secretion of adipokines [14, 15]; is a reservoir for VD; and, besides, can activate/inactivate it by hydroxylation. VD and VDR are implicated in preadipocyte differentiation into adipocytes [16].

Major differences between subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) were shown in the expression of VD-metabolizing enzymes. The expression of the VDR, 25-hydroxyvitamin D 1α-hydroxylase (CYP27B1) genes, and 24-hydroxylase enzymes has been shown in human adipocytes [17].

In line, our chapter will focus on VD status and expression of VDR and VD hydroxylase enzymes in SAT and VAT in an obese environment.
