| First Author | Li Y | Year | 2026 |
| Journal | PLoS Biol | Volume | 24 |
| Issue | 3 | Pages | e3003700 |
| PubMed ID | 41779769 | Mgi Jnum | J:391827 |
| Mgi Id | MGI:8296388 | Doi | 10.1371/journal.pbio.3003700 |
| Citation | Li Y, et al. (2026) Gpc3 selectively suppresses subcutaneous adipogenesis in diet-induced obesity. PLoS Biol 24(3):e3003700 |
| abstractText | Subcutaneous and visceral adipose depots employ distinct expansion strategies in response to dietary cues, yet the molecular regulators underlying these depot-specific adaptations remain poorly understood. Through integrated proteomic profiling of human subcutaneous and visceral adipose tissues from paired obese/non-obese donors and temporal transcriptomic analysis of mouse adipose stem and progenitor cells (ASPCs) during dietary transitions, we identified Glypican 3 (Gpc3) as an obesity-responsive gene exhibiting reciprocal expression patterns between depots. ASPC-specific Gpc3 deletion in mice amplified high-fat diet-induced weight and fat mass gain, with a selective enhancement of expansion in inguinal white adipose tissue (WAT) without affecting epididymal WAT. Mechanistically, Gpc3 loss biased ASPC fate toward adipogenesis over proliferation through depot-specific modulation of canonical Wnt signaling. These findings establish Gpc3 as a regulator for regional adipose plasticity, offering a molecular target for reprogramming pathological fat distribution in obesity and related metabolic disorders. |
