In this chapter, we define obesity as a condition resulting from the excessive accumulation of WAT, which significantly elevates the risk of numerous non-communicable diseases. Adipocytes, the primary cellular constituents of adipose tissue, and adipogenesis, the critical process of fat cell formation, will be examined in detail. Upon receiving specific signals, such as exposure to low temperatures, white adipocytes can convert to beige adipocytes, exhibiting characteristics akin to brown adipocytes. During the progression of overweight and obesity, adipocytes initially increase in size (hypertrophy) and subsequently in number (hyperplasia), which recruits a substantial influx of M1-type macrophages. These macrophages, along with T cells, form the major stromal-vascular fraction of adipose tissue, potentially leading to chronic inflammation within the tissue. We will explore the significant impact of adipokines during WAT hypertrophy and hyperplasia, particularly in their role in communicating with the CNS. Investigations into monogenic forms of obesity provide compelling evidence for the central role of appetite regulation in obesity susceptibility, with the leptin-melanocortin pathway playing a crucial role in satiety signaling. Variations in the genes associated with this pathway, along with numerous other genetic factors, will be discussed as key contributors to common obesity within the context of the modern obesogenic environment.