CoChat
Sign Up
Cited by 1,379Adipose Tissue and MetabolismMitochondrial Function and PathologyRegulation of Appetite and Obesity

Mice lacking mitochondrial uncoupling protein are cold-sensitive but not obese

Enerbäck, Sven, Jacobsson, Anders, Simpson, Elizabeth M., Guerra, Carmen, Yamashita, Hitoshi, Harper, Mary-Ellen, Kozak, Leslie P.·1997·Nature
DOI 10.1038/387090a0
Open this paper in CoChat — free account

Abstract

The mitochondrial uncoupling protein (UCP) in the mitochondrial inner membrane of mammalian brown adipose tissue generates heat by uncoupling oxidative phosphorylation. This process protects against cold and regulates energy balance. Manipulation of thermogenesis could be an effective strategy against obesity. Here we determine the role of UCP in the regulation of body mass by targeted inactivation of the gene encoding it. We find that UCP-deficient mice consume less oxygen after treatment with a beta3-adrenergic-receptor agonist and that they are sensitive to cold, indicating that their thermoregulation is defective. However, this deficiency caused neither hyperphagia nor obesity in mice fed on either a standard or a high-fat diet. We propose that the loss of UCP may be compensated by UCP2, a newly discovered homologue of UCP; this gene is ubiquitously expressed and is induced in the brown fat of UCP-deficient mice.

Integrity signals

Registry

Crossref · 10.1038/387090a0

Cites

32 of 32 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • 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 [40]

  • UCP1-deficient mice are cold sensitive.

    “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 [31]

  • 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 [31]

  • UCP1-ablated mice are more susceptible to cold and have to rely on shivering for thermoregulation.

    “Thus, UCP1-ablated mice are more susceptible to cold and have to rely on shivering for thermoregulation 31.”

    From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [31]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Enerbäck, S., Jacobsson, A., Simpson, E. M., Guerra, C., Yamashita, H., Harper, M.-E., & Kozak, L. P.
Affiliations
  • Jackson Laboratory (US)
  • Stockholm University (SE)
  • University of Ottawa (CA)
ORCID
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
1997-05
Volume
387
Issue
6628
Pages
90-94
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
DOI
10.1038/387090a0
OpenAlex
W2062073832
Cited by
1,379
References
32
Citations by year
2026: 25 · 2025: 26 · 2024: 50 · 2023: 53 · 2022: 49 · 2021: 56 · 2020: 61 · 2019: 52 · 2018: 63 · 2017: 55 · 2016: 60 · 2015: 73 · 2014: 53 · 2013: 56 · 2012: 34
FWCI
28.95
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Keywords
mitochondrial uncoupling proteins, UCP1, UCP2, brown adipose tissue, thermogenesis, cold sensitivity, thermoregulation, obesity, energy balance, oxygen consumption, beta3-adrenergic agonists, hyperphagia, high-fat diet, knockout mice, compensatory gene expression
MeSH terms
Uncoupling Protein 2, Uncoupling Protein 1, Adrenergic beta-Agonists, Animals, Body Temperature Regulation, Body Weight, Adipose Tissue, Brown, Carrier Proteins, Cold Temperature, Diet, Dioxoles, Female, Ion Channels, Male, Membrane Proteins, Mice, Transgenic, Mitochondria, Obesity, Oxygen Consumption, Proteins, Stem Cells, Uncoupling Agents, Gene Targeting, Mitochondrial Proteins, Membrane Transport Proteins, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review