Obesity is a multifactorial condition. Environmental risk factors related t
o a sedentary lifestyle and unlimited access to food apply constant pressur
e in subjects with a genetic predisposition to gain weight. The fact that g
enetic defects can result in human obesity has been unequivocally establish
ed over the past 3 years with the identification of the genetic defects res
ponsible for different monogenic forms of human obesity: the leptin, leptin
receptor, pro-opiomelanocortin, pro-hormone convertase-1 and melanocortin-
4 receptor genes. The common forms of obesity are, however, polygenic. The
examination of specific genes for involvement in the susceptibility to comm
on obesity has not yet yielded convincing results. Approaches involving the
candidate genes and the positional cloning of major obesity-linked regions
(state-of-the-art future prospects) will be discussed.