ABSTRACT
In addition to the many mouse models of obesity caused by spontaneous mutations, gene knockouts and gene insertions, the commonly used inbred laboratory strains of mice constitute the primary mammalian model system and are an integral component of obesity research. Within these lines, and their derivatives such as recombinant inbred lines, genome-wide congenic strains, chromosome substitution lines, advanced intercross lines, long-term selection lines, and heterogeneous stocks (HS) there exists a vast array of obesity-relevant genetic and phenotypic variation. The study of such variation, in the form of complex trait analysis including candidate gene analysis, quantitative trait loci (QTL)/eQTL mapping, and systems biology, has shed significant light on the genetic and genomic architecture of nearly all aspects of energy balance regulation and how body weight and body fat are controlled.
