Evolution of UCP1
Abstract
Brown adipose tissue (BAT), the specialized heat-producing organ found in many placental mammals including humans, may be accessible for clinical drug intervention to help combat metabolic diseases. Understanding the biology of BAT and its thermogenic uncoupling protein 1 (UCP1) will benefit from an assessment of its evolution, answering where UCP1 originated and how it has been modified and integrated into cellular energy metabolism. Here, we review topical insights regarding the molecular evolution of UCP1-also reconstructing the proximate and ultimate factors selecting for brown fat thermogenesis in placental mammals. This new thinking on "old" events will assist our understanding of how thermogenic mitochondrial uncoupling was integrated into the physiology of the brown adipocyte. Recent comparative studies examining the occurrence of UCP1 in vertebrates not only identified the ancient (pre-mammal) rise of UCP1 but also its repeated downfall during mammalian evolution as evidenced by multiple independent gene loss and/or inactivation events. Together with the comparative physiology of various species, we may be able to find conditions that favor UCP1 thermogenesis and, learning from these insights, identify molecular networks that will be useful to pharmacologically stimulate the tissue.
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Pangolins lack UCP1 and therefore cannot implement non-shivering thermogenesis.
“Pangolins also lack UCP1 (Gaudry et al., 2018) and therefore cannot implement non-shivering thermogenesis.”
From Temminck’s pangolins relax the precision of body temperature regulation when resources are scarce in a semi-arid environment (2023) · cites this paper as Gaudry et al., 2018
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Mitochondria: the birth place, battle ground and the site of melatonin metabolism in cells
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“UCP1 is exclusively present in the mitochondria of brown adipose tissue (118); other family members (homologs) of UCPs including UCPs 2-5 are distributed in the mitochondria of different”
BackgroundPanaino, W., Parrini, F., Kamerman, P. R., Hetem, R. S., Meyer, L. C. R., Smith, D., van Dyk, G., & Fuller, A. (2023) · Conservation Physiology · doi:10.1093/conphys/coad068 · Cited by 12 · see citing works
- Authors
- Gaudry, M. J., Campbell, K. L., & Jastroch, M.
- Affiliations
- University of Manitoba (CA)
- Helmholtz Munich (DE)
- Corresponding author
- Jastroch, Martin
- Venue
- Handbook of Experimental Pharmacology
- Publisher
- Springer International Publishing
- Published
- 2018
- Volume
- 251
- Pages
- 127-141
- ISSN
- 0171-2004 (ISSN-L)
- 1865-0325
- OpenAlex
- W2801729287
- Cited by
- 24
- References
- 7
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 4 · 2023: 4 · 2022: 2 · 2021: 5 · 2020: 3 · 2019: 4
- FWCI
- 10.07
- Type
- book chapter
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Handbook of experimental pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Site cant be reached (submittedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Physical Sciences › Environmental Science › Ecology › Physiological and biochemical adaptations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- UCP1, brown adipose tissue, thermogenesis, molecular evolution, placental mammals, mitochondrial uncoupling, brown adipocytes, gene loss, comparative physiology, energy metabolism
- MeSH terms
- Uncoupling Protein 1, Animals, Adipose Tissue, Brown, Female, Humans, Ion Channels, Pregnancy, Thermogenesis, Mitochondrial Proteins
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