Adipose Tissue-Specialized Immunologic Features Might Be the Potential Therapeutic Target of Prospective Medicines for Obesity

Figure 1

The AMPK and JNK signaling pathways are shown above. Besides the circulatory regulation of AMPK-SIRT1-LKB1, AMPK indirectly regulates NF-κB p65 by SIRT1. Additionally, AMPK might induce the association of PGC-1α. The interaction of NF-κB and IκB might result in nuclear accumulation and activation of NF-κB, leading to IL-10, IL-1β, and IL-6 transcriptions and expressions. Likewise, TNF-α inhibits AMPK via upregulation of protein phosphatase 2C (PP2C). In the JNK signaling pathway, the main pathway is that TNF-α activates Map4k4 by combining with TNFR1 to inhibit PPARγ. Nevertheless, TNF-α activates NF-κB by phosphorylation of JNK1/2. PPARγ might block the interaction of NF-κB and IκB.