Figure 1. The relationship between the core clock mechanism and metabolic factors. CLOCK and BMAL1 mediate the ... Figure 1. The relationship between the.

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Figure 1. The relationship between the core clock mechanism and metabolic factors. CLOCK and BMAL1 mediate the ... Figure 1. The relationship between the core clock mechanism and metabolic factors. CLOCK and BMAL1 mediate the expression of clock- and clock-controlled genes regulating metabolism. PER1, PER2, and CRY1 serve as the negative-feedback loop that inhibits CLOCK:BMAL1-mediated expression. The catabolic factors SIRT1, PGC1, and AMPK, when activated under low cellular energy levels, relieve the inhibition mediated by the negative-feedback loop. BMAL1 expression is positively regulated by RORs and PPARs and negatively regulated by reverse ERBs (REV-ERBs). mTOR, an anabolic factor, interacts with BMAL1 and suppresses the activity of the catabolic factors. The green arrows and red lines denote possible pathways that activate or inhibit adipocyte metabolism, respectively. Unless provided in the caption above, the following copyright applies to the content of this slide: Copyright © 2018 Endocrine Society Endocr Rev, Volume 39, Issue 3, 27 February 2018, Pages 261–273, https://doi.org/10.1210/er.2017-00193 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 2. Lineage of white, brown, and “brite/beige” adipocytes from mesenchymal stem cells and their cellular and ... Figure 2. Lineage of white, brown, and “brite/beige” adipocytes from mesenchymal stem cells and their cellular and molecular markers. Myf5, myogenic factor 5. Unless provided in the caption above, the following copyright applies to the content of this slide: Copyright © 2018 Endocrine Society Endocr Rev, Volume 39, Issue 3, 27 February 2018, Pages 261–273, https://doi.org/10.1210/er.2017-00193 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 4. The relationship between the core clock mechanism and differentiation signaling pathways in BAT and WAT. ... Figure 4. The relationship between the core clock mechanism and differentiation signaling pathways in BAT and WAT. BMAL1 activates the transcription of PPARγ and PER2. PER2 inhibits BMAL1 activity, and PPARγ increases BMAL1 expression. Wnt signaling represses WAT adipogenesis, whereas TGFβ/Smad3 signaling represses BAT formation. BMP signaling induces BAT formation. Reduced levels of BMAL1 lead to increased WAT and BAT formation. Unless provided in the caption above, the following copyright applies to the content of this slide: Copyright © 2018 Endocrine Society Endocr Rev, Volume 39, Issue 3, 27 February 2018, Pages 261–273, https://doi.org/10.1210/er.2017-00193 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 3. Temporal expression of adipocytokines in rodents and humans Figure 3. Temporal expression of adipocytokines in rodents and humans. The peak expression of each adipokine is ... Figure 3. Temporal expression of adipocytokines in rodents and humans. The peak expression of each adipokine is depicted. Representation of the acrophase or timing of the maximum levels of adipokine expression in human adipose tissue: comparison with human circulating levels and with rodent adipose tissue mRNA levels. Data are represented as the 5 hours of active and resting phase in both humans and rodents, as this is the timing when most adipokines peak. IL-6, interleukin 6; PAI-1, plasminogen activator inhibitor 1; PPAR, peroxisome proliferator–activated receptor. Unless provided in the caption above, the following copyright applies to the content of this slide: Copyright © 2018 Endocrine Society Endocr Rev, Volume 39, Issue 3, 27 February 2018, Pages 261–273, https://doi.org/10.1210/er.2017-00193 The content of this slide may be subject to copyright: please see the slide notes for details.