Are 'set points' a real biological factor

Introduction
We don't get fat only because we eat too much and move too little. In actuality, small doses of the wrong foods and short periods of inactivity can lead to new "set points" (aka homostasis) at which the hormonal and regulatory mechanisms of the body compensate.

In healthy people reducing energy in and increasing energy out works exactly as predicted: the energy deficit is provided by body stores. In healthy people, homeostasis ensures that we get fat when food is abundant and lean out when food is scarce. For the obese, however, people who have been overweight for many years, homeostatic mechanisms can become broken. This is when insulin resistance leads to metabolic syndrome. The same can happen with leptin, the hypothalamus can stop sensing changes in leptin. And the same can happen for any of the other hormones and signalling mechanisms.

Arguments for
Body weight homeostasis are the biological processes which govern the long-term behaviour of our bodies, which are themselves influenced by genes and hormones. changes in the rates of expression of these hormones can take weeks or months to re-adjust to new environmental conditions, for example a new diet.

Weight gain is a response to over eating, and not moving enough. These environmental conditions are resolved by the body by, for example, converting excess energy in order to convert carbohydrates to fat. This is expressed as insulin resistance, which is an adaptive response to a toxic environment. This is the biological mechanism bears use to store fat in the winter.

Weight loss reduces leptin signalling from fat cells. When a fat cell is full, it gives off leptin. When that cell has capacity to store more fat it stops producing leptin. The fuller your fat cells are, the more leptin your adipose tissue is producing. Leptin signals that there is enough fat already. This works well to suppress appetite, unless you become leptin resistant, or are naturally leptin insensitive.

Acute leptin deficiency, leptin resistance, and the physiologic response to leptin withdrawal http://www.ncbi.nlm.nih.gov/pmc/articles/PMC548993/