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Obesity-induced elevated palmitic acid promotes inflammation and glucose metabolism disorders through GPRs/NF-κB/KLF7 pathway by Tongtong Qiu; Xin Yang; Jingzhou Wang; Chongge Pan; Xiaolong Chu; Jianyu Xiong; Jianxin Xie; Yongsheng Chang; Cuizhe Wang; Jun Zhang is a Medicine article available to read on EtoBox.

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## Objective Our previous results have shown that obesity-induced excessive palmitic acid (PA) can promote the expression of KLF7, which plays a vital role in regulation of inflammation, glucose metabolism. But the exact mechanism of PA up-regulating the expression of KLF7 is not clear yet. This study is intend to explore whether PA promoting KLF7 expression through GPRs/NF-κB signaling pathway, causing inflammation and glucose metabolism disorders. ## Methods Cells were blocked GPRs/NF-κB under PA stimulation in vitro to demonstrate the molecular mechanism of PA up-regulates KLF7 expression. The regulatory effect of p65 on KLF7 was detected by luciferase reporter gene assay. Blocking GPRs/NF-κB in diet-induced obesity mice to detect the expression of KLF7, inflammatory cytokines and glucose metabolism related factors, clarifying the effects of GPRs/NF-κB on KLF7 in vivo. ## Results In 3T3-L1 adipocytes and HepG2 cells, PA could up-regulate the expression of KLF7 by promoting the GPR40/120-NF-κB signaling pathway, leading to inflammation and reduced glucose consumption (__p__ < 0.05 for both). Luciferase reporter gene assay and ChIP assay showed that p65 could transcriptionally up-

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Author

Tongtong Qiu; Xin Yang; Jingzhou Wang; Chongge Pan; Xiaolong Chu; Jianyu Xiong; Jianxin Xie; Yongsheng Chang; Cuizhe Wang; Jun Zhang

Publisher

Springer Science and Business Media LLC

Published

2022

Language

EN

Field

Medicine (Health Sciences)