ABSTRACT
Brown adipose tissue (BAT) is responsible for adaptive thermogenesis. We previously showed that genetic deficiency ofreceptor for advanced glycation end products (RAGE) prevented the effects of high-fat diet (HFD). This study was tocompare BAT activity in RAGE knock out (Ager-/-, RKO) and wild-type (WT) mice after treated with HFD or LFD.[18F]FDG PET-CT imaging under identical cold-stimulated conditions and mean standard uptake values (SUVmean), ratio ofSUViBAT/SUVmuscle (SUVR, muscle as the reference region) and %ID/g were used for BAT quantification. The resultsshowed that [18F]FDG uptake (e.g., SUVR) in WT-HFD mice was significantly reduced (three-fold) as compared to that inWT-LFD (1.40 ± 0.07 and 4.03 ± 0.38; P = 0.004). In contrast, BAT activity in RKO mice was not significantly affectedby HFD, with SUVRRKO-LFD: 2.14 ± 0.10 and SUVRRKO-LFD: 1.52 ± 0.13 (P = 0.3). The uptake in WT-LFD was almostdouble of that in RKO-LFD (P = 0.004); however, there was no significant difference between RKO-HFD and WT-HFDmice (P = 0.3). These results, corroborating our previous findings on the measurement of mRNA transcripts for UCP1 inthe BAT, suggest that RAGE may contribute to altered energy expenditure and provide a protective effect against HFD byAger deletion (Ager -/-).