ABSTRACT
A major role for genotype in the development of obesity is supported by data from twin, adoption, and population studies. Since it is likely that obesity is polygenic in man — or at least that different genes are responsible in different families — segregation analysis of families from diverse genetic backgrounds is unlikely to be fruitful. The application of the polymerase chain reaction to segments of DNA which are highly polymorphic within populations has allowed the rapid construction of complete maps of the human, mouse, and rat genomes. The autosomal recessive mutations which result in obesity in mice and rats reflect loss of function in genes which must act normally to suppress the body weight by effects on both food intake and energy expenditure. Detailed molecular genetic maps of the regions containing mouse obesity mutations can be exploited in several ways. Thus, diseases which are the result of multiple, interacting genes can be dissected genetically.
