| First Author | Rahbani JF | Year | 2024 |
| Journal | Cell Metab | Volume | 36 |
| Issue | 3 | Pages | 526-540.e7 |
| PubMed ID | 38272036 | Mgi Jnum | J:345951 |
| Mgi Id | MGI:7610115 | Doi | 10.1016/j.cmet.2024.01.001 |
| Citation | Rahbani JF, et al. (2024) Parallel control of cold-triggered adipocyte thermogenesis by UCP1 and CKB. Cell Metab 36(3):526-540.e7 |
| abstractText | That uncoupling protein 1 (UCP1) is the sole mediator of adipocyte thermogenesis is a conventional viewpoint that has primarily been inferred from the attenuation of the thermogenic output of mice genetically lacking Ucp1 from birth (germline Ucp1(-/-)). However, germline Ucp1(-/-) mice harbor secondary changes within brown adipose tissue. To mitigate these potentially confounding ancillary changes, we constructed mice with inducible adipocyte-selective Ucp1 disruption. We find that, although germline Ucp1(-/-) mice succumb to cold-induced hypothermia with complete penetrance, most mice with the inducible deletion of Ucp1 maintain homeothermy in the cold. However, inducible adipocyte-selective co-deletion of Ucp1 and creatine kinase b (Ckb, an effector of UCP1-independent thermogenesis) exacerbates cold intolerance. Following UCP1 deletion or UCP1/CKB co-deletion from mature adipocytes, moderate cold exposure triggers the regeneration of mature brown adipocytes that coordinately restore UCP1 and CKB expression. Our findings suggest that thermogenic adipocytes utilize non-paralogous protein redundancy-through UCP1 and CKB-to promote cold-induced energy dissipation. |
