Adipocyte count is essential to maintaining weight.

It is unclear to what extent weight is genetic rather than environmentally set at a later stage in development.

Given that in adulthood adipocyte number stays constant, and weight changes are predominantly accompanied by changes in adipocyte volume, one may conclude that at some critical point in development the final fat cell number is attained and after this point no fat cell turnover occurs. Analysis of adipocyte turnover using carbon-14 dating (for a detailed methodological description, see Ref. [5]), however, has recently shown that this is not the case, but rather that adipocytes are a dynamic and highly regulated population of cells. New adipocytes form constantly to replace lost adipocytes, such that approximately every 8 years 50% of adipocytes (...) are replaced (emphasis added).

I am unable to find whether fat cell count can be changed over this 8 year time scale, though my biochemistry professor was inclined to that hypothesis.

Obesity can be characterised into two main types, hyperplastic (increase in adipocyte number) and hypertrophic (increase in adipocyte volume). Obese and overweight individuals may exist anywhere along the cellularity scale, however on average certain trends appear. Hypertrophy, to a degree, is characteristic of all overweight and obese individuals. Hyperplasia, however, is correlated more strongly with obesity severity.

Heredity and weight:

at present, it is impossible to conclude whether the average increase in adipocyte number seen in obese and severely obese individuals is the result of adult adipocyte recruitment or rather a reflection of a population of people predisposed (by their pre-adulthood fat cell number) to be become obese/severely obese.

The long-term weight loss cited in this review used a 1-2 year followup, during which time only <16% of adipocytes could have turned over.

it is clear that fat cell number does not decrease in adulthood, even following long-term weight loss. (emphasis added) In line with this, hyperplastic obese individuals have a poorer treatment outcome following diet-induced weight loss than hypertrophic individuals (when controlled for fat mass). Often for hyperplastic obese individuals, treatments other than diet and exercise are necessary if substantial and permanent weight loss is to be achieved. Successful, but invasive therapies include surgery to reduce the amount of calories ingested (e.g. gastric bypass) and/or surgical removal of fat tissue (e.g. reconstructive surgery or liposuction). The recent discovery of a high turnover of adipocytes in adult human white adipose tissue (approximately 10% annually) now establishes an additional therapeutic target for the pharmacological intervention of obesity [1].