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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Trends Endocrinol Metab. 2015 Mar 21;26(5):248–255. doi: 10.1016/j.tem.2015.02.006

Figure 2. Notch signaling regulates adipocyte thermogenesis.

Figure 2

In response to cold ambient temperature, sympathetic nervous system releases catecholamine, which binds with β-adrenergic receptor and activates lipolysis through the cAMP pathway. Fatty acids (FAs) can directly activate uncoupling protein 1 (UCP1) for heat production. Notch target gene Hes1 directly binds to the promoter region of Prdm16, Ppargc1a and Pparγ, and inhibit their transcription. This leads to reduced mitochondria numbers and expression of UCP1. Notch signaling promotes activation and production of proinflammatory cytokines mediated by NF-κB, which attracts macrophages and together cause low-grade systematic inflammation and exacerbates insulin resistance. In obesity, infiltrated macrophages activate transcription of Notch ligand Dll4 through NF-κB. Dotted line indicates indirect effect. IL-1β, interleukin 1β; TNFα, tumor necrosis factor α; IL-1R, interleukin 1 receptor; TNFR, tumor necrosis factor receptor; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; Dll4, delta-like 4; Pparγ, peroxisome proliferator-activated receptor gamma; PGC1α, Pparγ coactivator 1-alpha; Prdm16, PR domain containing 16;.