| First Author | Gallo R | Year | 2024 |
| Journal | iScience | Volume | 27 |
| Issue | 7 | Pages | 110259 |
| PubMed ID | 39027371 | Mgi Jnum | J:351625 |
| Mgi Id | MGI:7702939 | Doi | 10.1016/j.isci.2024.110259 |
| Citation | Gallo R, et al. (2024) IL-17A produced by POMC neurons regulates diet-induced obesity. iScience 27(7):110259 |
| abstractText | Overeating leads to obesity, a low-grade inflammatory condition involving interleukin-17A (IL-17A). While pro-opiomelanocortin (POMC) neurons regulate feeding, their connection with IL-17A is not well understood. To impair IL-17A signaling in POMC neurons, IL-17A receptor (Il17ra) was deleted by crossing IL17ra-flox and Pomc-Cre mice. Despite effective deletion, these mice showed no differences in body weight or adiposity compared to control mice, challenging the idea that IL-17A induces obesity through POMC neuron regulation. However, both groups exhibited reduced weight gain and adiposity upon high-fat diet compared to mice carrying only the floxed alleles, suggesting independent effects of Pomc-Cre transgene on body weight. Further analysis reveals that POMC neurons express IL-17A, and reduction in number of POMC neurons in Pomc-Cre mice could be linked to decreased IL-17A expression, which correlates with reduced adipocyte gene expression associated with obesity. Our data underscore an unexpected crosstalk between IL-17A-producing POMC neurons and the endocrine system in obesity regulation. |
