Abstract
In this chapter, we will define obesity as the consequence of excess WAT accumulation that increases the risk of non-communicable diseases. We will describe adipocytes as the central cellular component of adipose tissue and adipogenesis as the key process creating fat cells. In response to appropriate signals, such as low temperature, white adipocytes are able to transform to beige adipocytes displaying a phenotype similar to brown adipocytes. During the development of overweight and obesity, adipocytes first grow in size and then in number attracting many M1-type macrophages. The latter form together with T cells the major stromal-vascular fraction of adipose tissue and can lead to chronic inflammation in the tissue. We will show that adipokines have a major impact during hypertrophy and hyperplasia of WAT and for the communication with the CNS. Studying monogenic forms of obesity provides strong evidence for a central role of appetite regulation in obesity susceptibility. The leptin-melanocortin pathway has an integral role in this satiety signaling. Variations in genes of this pathway as well as numerous others will be presented as important drivers of common obesity in context of the modern obesogenic environment.