| First Author | Phuong NQ | Year | 2025 |
| Journal | Sci Rep | Volume | 15 |
| Issue | 1 | Pages | 941 |
| PubMed ID | 39824986 | Mgi Jnum | J:361527 |
| Mgi Id | MGI:7858512 | Doi | 10.1038/s41598-024-81917-7 |
| Citation | Phuong NQ, et al. (2025) Role of transforming growth factor-beta1 in regulating adipocyte progenitors. Sci Rep 15(1):941 |
| abstractText | Adipose tissue (AT) metabolism involves coordinating various cells and cellular processes to regulate energy storage, release, and overall metabolic homeostasis. Therein, macrophage and its cytokine are important in controlling tissue homeostasis. Among cytokines, the role of transforming growth factor-beta1 (Tgf-beta1), a cytokine abundantly expressed in CD206(+) M2-like macrophage and correlated with the expansion of AT and fibrosis, in AT metabolism, remains unknown. We used CD206CreER(T2); Tgf-beta1(f/f) mouse model in which the Tgf-beta1 gene was conditionally deleted in CD206(+) M2-like macrophages followed by tamoxifen administration, to investigate the role of the Tgf-beta1 gene in glucose and insulin metabolism. Our data demonstrated that lack of CD206(+) M2-like macrophages derived Tgf-beta1 gene improved glucose metabolism and insulin sensitivity by enhancing adipogenesis via hyperplasia. The Tgf-beta1 gene, specifically from CD206(+) M2-like macrophages, deletion stimulated APs' proliferation and differentiation, leading to the generation of smaller mature adipocytes, therefore enhancing insulin sensitivity and improving glucose metabolism under normal chow conditions. Our study brings a new perspective that Tgf-beta1 gene deletion specific from CD206(+) M2-like macrophage promotes adipocyte hyperplasia, improving glucose homeostasis and insulin sensitivity in the lean state. |
