It might be easier to think of it in terms of an individual's adipogenic capacity (i.e. your upper potential/threshold for fat cells).
White adipose tissue (WAT) is a dynamic and modifiable tissue that develops late during gestation in humans and through early postnatal development in rodents. WAT is unique in that it can account for as little as 3% of total body weight in elite athletes or as much as 70% in the morbidly obese. With the development of obesity, WAT undergoes a process of tissue remodeling in which adipocytes increase in both number (hyperplasia) and size (hypertrophy). Metabolic derangements associated with obesity, including type 2 diabetes, occur when WAT growth through hyperplasia and hypertrophy cannot keep pace with the energy storage needs associated with chronic energy excess. Accordingly, hypertrophic adipocytes become overburdened with lipids, resulting in changes in the secreted hormonal milieu. Lipids that cannot be stored in the engorged adipocytes become ectopically deposited in organs such as the liver, muscle, and pancreas. WAT remodeling coincides with obesity and secondary metabolic diseases.
An interesting debate within bariatric surgery is if bariatric surgery and long term caloric restriction can change the number of adipose-derived stromal/progenitor cells that would otherwise give rise to new adipocytes based on your genetic adipogenic capacity.