Parallel control of cold-triggered adipocyte thermogenesis by UCP1 and CKB
Copyright © 2024 Elsevier Inc. All rights reserved..
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.
| Errataetall: |
CommentIn: Cell Metab. 2024 Mar 5;36(3):459-460. - PMID 38447527 |
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| Medienart: |
E-Artikel |
| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:36 |
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| Enthalten in: |
Cell metabolism - 36(2024), 3 vom: 05. März, Seite 526-540.e7 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Rahbani, Janane F [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 08.03.2024 Date Revised 20.03.2024 published: Print-Electronic CommentIn: Cell Metab. 2024 Mar 5;36(3):459-460. - PMID 38447527 Citation Status MEDLINE |
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| doi: |
10.1016/j.cmet.2024.01.001 |
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| Förderinstitution / Projekttitel: |
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| 520 | |a 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 | ||
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| 700 | 1 | |a Samborska, Bozena |e verfasserin |4 aut | |
| 700 | 1 | |a Roesler, Anna |e verfasserin |4 aut | |
| 700 | 1 | |a Xiao, Haopeng |e verfasserin |4 aut | |
| 700 | 1 | |a Shaw, Abhirup |e verfasserin |4 aut | |
| 700 | 1 | |a Kaiser, Zafir |e verfasserin |4 aut | |
| 700 | 1 | |a Braun, Jessica L |e verfasserin |4 aut | |
| 700 | 1 | |a Geromella, Mia S |e verfasserin |4 aut | |
| 700 | 1 | |a Fajardo, Val A |e verfasserin |4 aut | |
| 700 | 1 | |a Koza, Robert A |e verfasserin |4 aut | |
| 700 | 1 | |a Kazak, Lawrence |e verfasserin |4 aut | |
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