Someone asked me a question about how much genetics play a role in being fat, so I thought I'd post my response to him here:
Not much.
Not considering clinically diagnosed hypo- or hyper- thyroidism, the difference in metabolic rate, between two similar individuals, is around 500-600 cals, at the very most. On average, probably around 100-300 range. Thus, in most cases, no, genetics do not play a significant role at all in losing fat.. it's still governed by thermodynamics, as usual. Deleterious sequelae as a result of chronic obesity, and ergo myriad metabolic derangements, can however override these rules, to an extent. For instance, chronic obesity will lead to leptin resistance, thus the main long-term signal for satiety, plus a main hormone/adipokine in increasing/regulating metabolic rate (via catechomaines & thyroid hormones), is now unable to exert its usual effect. Another example, which also feeds into the aforementioned pathway, includes a robust cortisol response. Once the leptin resistance, and other similar perturbations occur, and your satiety signals are attenuated, you will most likely continue to overeat. Cortisol is typically lipolytic, however, in the presence of insulin, especially mass fluxes you would expect in the chronic obese patient (overeating/high CHO foods, insulin resistance), it will augment the fat storage/lipogenesis capabilities.
Now, there are instances of actual genetic mutations, exorbitantly increasing incidence/risk/severity of obesity. Important here are SNPs (single nucleotide polymorphisms), which are the exact, ubiquitous mutations that are pertinent here (amongst a few other, rarer forms). There are a few particularly common mutations that appear to cause obesity, either directly or indirectly (apart from hypo-thyroidism), such as mutations in the melanocortin 4 receptor, prohormone convertase, brain-derived neurotrophic factor (BDNF), etcetera. These, and the few other common mutations, are all typically involved in either signaling for satiety, or in producing metabolic hormones themselves (so, leptin/melanocortin pathways). Or with BDNF - reward behavior with eating.
The melanocortin 4 receptor polymorphisms seem to account for roughly 6% of all cases of obesity.. but again, that's already a small amount of the total population (IIRC I read it was a bit less than 2% or something, but I may be off), making it incredibly uncommon.. but on the flip-side, not terribly uncommon in those actually obese, considering. I don't know about the rest. I wouldn't really consider these too pertinent for typical conversation dealing with fat loss, though. These are clearly rare.. my example is, I believe, by far the most abundant.
So, tl;dr - most likely not worth considering the genetic contribution to fat loss/obesity.