Variants of the human intestinal fatty acid binding protein 2 gene (FABP2) are 
associated with traits of the metabolic syndrome. Relevant FABP2 promoter 
polymorphisms c.-80_-79insT, c.-136_-132delAGTAG, c.-168_-166delAAGinsT, 
c.-260G>A, c.-471G>A, and c.-778G>T result in two haplotypes A and B. Activation 
of haplotypes by rosiglitazone stimulated PPARgamma/RXRalpha leads to 2-fold 
higher activity of haplotype B than A. As shown by chimeric FABP2 promoter 
constructs, the higher responsiveness of FABP2 haplotype B is mainly but not 
solely determined by polymorphism c.-471G>A. As shown by EMSA and 
promoter-reporter assays, Oct-1 interacts with the -471 region of FABP2 
promoters, induces the activities of both FABP2 promoter haplotypes and 
abolishes the different activities of haplotypes induced by rosiglitazone 
activated PPARgamma/RXRalpha. In conclusion, our findings suggest a functional 
role of PPARgamma/RXRalpha and Oct-1 in the regulation of the FABP2 gene.