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Cited by 1,318Adipose Tissue and MetabolismRegulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic Diseases

UCP1 Ablation Induces Obesity and Abolishes Diet-Induced Thermogenesis in Mice Exempt from Thermal Stress by Living at Thermoneutrality

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Feldmann, Helena M., Golozoubova, Valeria, Cannon, Barbara, Nedergaard, Jan·2009·Cell Metabolism
DOI 10.1016/j.cmet.2008.12.014
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Abstract

As original studies of UCP1-ablated mice failed to demonstrate an obesogenic effect, alternative mechanisms for adaptive adrenergic thermogenesis have been sought. However, we demonstrate here that in C57Bl6 mice exempt from thermal stress (i.e., kept at thermoneutrality), UCP1 ablation in itself induced obesity, even in mice fed control diet, and vastly augmented diet-induced obesity (high-fat diet); i.e., the mice exhibited increased metabolic efficiency. In wild-type mice, high-fat diet increased norepinephrine-induced thermogenesis; i.e., diet-induced thermogenesis was observed, but no such effect was observed in UCP1-ablated mice, demonstrating that diet-induced thermogenesis fully emanates from UCP1 activity. We conclude that ambient temperature is qualitatively determinative for the outcome of metabolic studies, that no other protein and no other mechanism can substitute for UCP1 in mediating diet-induced adrenergic thermogenesis, and that UCP1 activity can be determinative for obesity development in mice and possibly in humans.

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  • Altered UCP1 expression (UCP1-deficient or transgenic mice) leads to dysregulated sensitivity to cold exposure and body weight control.

    “In fact, altered UCP1 expression (UCP1-deficient or transgenic mice) leads to dysregulated sensitivity to cold exposure and body weight control ([40](#B40), [42](#B42), [86](#B86), [87](#B87), [98](#B98)).”

    From Mitochondrial fatty acid oxidation in obesity (2013) · cites this paper as [42]

  • UCP1-deficient mice exhibit increased susceptibility to diet-induced obesity.

    “UCP1-deficient mice are cold sensitive 31 and exhibit increased susceptibility to diet-induced obesity 32,33.”

    From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [33]

  • Animal experiments have indicated an indispensible role of UCP1 in mediating both NST and DIT.

    “At the molecular level, animal experiments have indicated an indispensible role of UCP1 in mediating both NST and DIT.”

    From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [33]

  • When kept at thermoneutrality, UCP1 knockout mice lack DIT and develop obesity, indicating that diet-induced thermogenesis is fully dependent on UCP1.

    “When kept at thermoneutrality (30 °C for mice), UCP1 knockout mice lack DIT and develop obesity 33, indicating that diet-induced thermogenesis is fully dependent on UCP1.”

    From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [33]

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Authors
Feldmann, H. M., Golozoubova, V., Cannon, B., & Nedergaard, J.
Affiliations
Stockholm University (SE)
Corresponding author
Nedergaard, Jan
ORCID
Venue
Cell Metabolism
Publisher
Elsevier BV
Published
2009-02
Volume
9
Issue
2
Pages
203-209
ISSN
1550-4131 (ISSN-L)
DOI
10.1016/j.cmet.2008.12.014
OpenAlex
W2114821999
Cited by
1,318
References
33
Citations by year
2026: 32 · 2025: 45 · 2024: 56 · 2023: 80 · 2022: 76 · 2021: 81 · 2020: 93 · 2019: 81 · 2018: 102 · 2017: 95 · 2016: 98 · 2015: 98 · 2014: 90 · 2013: 80 · 2012: 72
FWCI
46.16
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • RVC Research Online (Royal Veterinary College) (submittedVersion, cc-by)
Funders
Institut National Du Cancer
Topics
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
UCP1, diet-induced thermogenesis, diet-induced obesity, thermoneutrality, ambient temperature, norepinephrine, brown adipose tissue, metabolic efficiency, obesity, high-fat diet
MeSH terms
Uncoupling Protein 1, Animals, Adipose Tissue, Brown, Eating, Energy Metabolism, Humans, Ion Channels, Mice, Inbred C57BL, Norepinephrine, Obesity, Receptors, Adrenergic, beta, Stress, Physiological, Temperature, Mice, Knockout, Thermogenesis, Mitochondrial Proteins, Mice

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