| First Author | Yang X | Year | 2023 |
| Journal | FASEB J | Volume | 37 |
| Issue | 7 | Pages | e23033 |
| PubMed ID | 37342904 | Mgi Jnum | J:341951 |
| Mgi Id | MGI:7541624 | Doi | 10.1096/fj.202300005R |
| Citation | Yang X, et al. (2023) KLF7 promotes adipocyte inflammation and glucose metabolism disorder by activating the PKCzeta/NF-kappaB pathway. FASEB J 37(7):e23033 |
| abstractText | In the obesity context, inflammatory cytokines secreted by adipocytes lead to insulin resistance and are key to metabolic syndrome development. In our previous study, we found that the transcription factor KLF7 promoted the expression of p-p65 and IL-6 in adipocytes. However, the specific molecular mechanism remained unclear. In the present study, we found that the expression of KLF7, PKCzeta, p-IkappaB, p-p65, and IL-6 in epididymal white adipose tissue (Epi WAT) in mice fed a high-fat diet (HFD) was significantly increased. In contrast, the expression of PKCzeta, p-IkappaB, p-p65, and IL-6 was significantly decreased in Epi WAT of KLF7 fat conditional knockout mice. In 3T3-L1 adipocytes, KLF7 promoted the expression of IL-6 via the PKCzeta/NF-kappaB pathway. In addition, we performed luciferase reporter and chromatin immunoprecipitation assays, which confirmed that KLF7 upregulated the expression of PKCzeta transcripts in HEK-293T cells. Collectively, our results show that KLF7 promotes the expression of IL-6 by upregulating PKCzeta expression and activating the NF-kappaB signaling pathway in adipocytes. |
