TRAP Induces Obesity Figure 6. Metabolic and inflammatory profile of adipose tissue from obese TRAP over expressing mice. (A) Levels of leptin and adiponectin mRNA and serum protein in WT and TRAP+ mice. (B) Inflammatory gene expression profile in the TRAP+ mice. (C) Noradrenalin- stimulated lipolysis in isolated adipocytes from TRAP+ and WT mice. (D) Insulin-inhibitable lipolysis in isolated adipocytes from TRAP+ and WT mice. (E) Insulin- stimulated lipogenesis in isolated adipocytes from TRAP+ and WT mice. (F) Levels of blood glucose and insulin in TRAP+ mice. doi:10.1371/journal.pone.0001713.g006 allele exists, it was acquired fortuitously in a complex breeding history from the original transgene, so the process clearly cannot be repeated precisely. This may pose a limitation to generate sublines of the desired phenotype, but since the original transgene construct gave very reproducible over-expression, new founders could be readily back-crossed to different inbred mouse strains to generate congenic strains in order to recapitulate the ‘‘obese’’ phenotype on more defined genetic backgrounds. We can assume that the corresponding ‘‘lean’’ allele could be identified genetically by performing a genome scan of a set of individual lean and fat individuals and a candidate genetic interval could be refined by intercrossing lean and fat sublines. It may also be that screening inbred mouse lines for a preponderance of monomeric TRAP could identify the genetic origin of the allele. Finally, comparative array profiling of macrophages from the two sub lines could also contribute to identification of a presumptive candidate modifier PLoS ONE | www.plosone.org 8 March 2008 | Volume 3 | Issue 3 | e1713