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Moreover, pockets of cells with the multilocular morphology characteristic of brown adipocytes ( Tsukiyama-Kohara et?al., 2001) were observed in RWAT ( Figure?2C). Immunohistochemical staining showed substantially higher levels of?UCP1 protein not only in the cells with typical brown fat morphology but also in some cells with unilocular white fat morphology surrounding the pocket of brown fat-like cells ( Figure?2C) ( Tsukiyama-Kohara et?al., 2001). Western blot showed marked increase of UCP1, mitochondrial protein HSP60, ��3AR, and PGC-1�� levels in RWAT of EE mice ( Figure?2D), consistent with the upregulation of mRNAs. Moreover, the mitochondrial DNA content of EE RWAT was increased by 2-fold, buy NU7441 indicating enhanced mitochondrial biogenesis ( Figure?2E) ( Xue et?al., 2007). The other two white fat pads, EWAT ( Figure?S2D) and IWAT ( Figure?S2E), showed fewer genetic changes compared to RWAT. However, expression of the major adipokine, leptin (Lep), was highly suppressed in all fat pads ( Figures 2A and 2B, Figures S2D and S2E), consistent with the observed sharp drop in leptin serum levels ATP7A (64.3%?�� 4.0% decrease). Although efficient in reducing adiposity, voluntary wheel running for 4?weeks induced different gene expression profiles in BAT and RWAT compared to EE. Running led to more robust changes in BAT than EE (Figure?2B). However, less BAT-selective genes were induced in RWAT of the running mice (Figure?2A). We analyzed the RWAT gene expression profiles after 10?weeks EE, wheel running, and EE without wheel. The standard EE induced the most robust BAT gene program in RWAT, while the effects of wheel running and EE without wheel were not additive (Figure?2F). The molecular signatures in fat induced by the different environmental interventions suggest distinctive molecular mechanisms underlying the reduction in adiposity in response to EE and running. EE induced a ��browning�� molecular signature in white fat suggesting that an individual's interaction Anti-infection Compound Library cost with its immediate environment could switch a white fat energy storage phenotype to a brown fat-like energy expenditure phenotype and regulate adiposity. To test this hypothesis, we investigated whether this transformation could help animals resist DIO. The chow was changed to a high-fat diet (HFD, 45% fat, caloric density 4.73?kcal/g) immediately after mice were randomly assigned to live in EE or control housing. After 4?weeks HFD feeding, the EE mice gained less weight (71.3%?�� 2.7% of control mice weight gain, Figures 3A and 3D) and remained lean with significantly smaller fat pads (p?
