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Cited by 1,075Adipose Tissue and MetabolismRegulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic Diseases

The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.

Development of obesity in transgenic mice after genetic ablation of brown adipose tissue

Lowell, Bradford B., S-Susulic, Vedrana, Hamann, Andreas, Lawitts, Joel A., Himms-Hagen, Jean, Boyer, Bert B., Kozak, Leslie P., Flier, Jeffrey S.·1993·Nature
DOI 10.1038/366740a0
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Abstract

Brown adipose tissue, because of its capacity for uncoupled mitochondrial respiration, has been implicated as an important site of facultative energy expenditure. This has led to speculation that this tissue normally functions to prevent obesity. Attempts to ablate or denervate brown adipose tissue surgically have been uninformative because it exists in diffuse depots and has substantial capacity for regeneration and hypertrophy. Here we have used a transgenic toxigene approach to create two lines of transgenic mice with primary deficiency of brown adipose tissue. At 16 days, both lines have decreased brown fat and obesity. In one line, brown fat subsequently regenerates and obesity resolves. In the other line, the deficiency persists and obesity, with its morbid complications, advances. Obesity develops in the absence of hyperphagia, indicating that brown fat deficient mice have increased metabolic efficiency. As obesity progresses, transgenic animals develop hyperphagia. This study supports a critical role for brown adipose tissue in the nutritional homeostasis of mice.

Overview

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Crossref · 10.1038/366740a0

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Citations

Cites

Research works printed but not linked: 6

  1. Rothwell, N. J. & Stock, M. J. Am. J. Physiol. 257, R253–R258 (1989).
  2. Breitman, M. L. & Bernstein, A. in Transgenic Animals (eds Grosveld, F. & Kollias, G.) 127–145 (Academic, Boston, 1992).
  3. Granneman, J. G., Lahners, K. N. & Chaudhry, A. Molec. Pharmac. 40, 895–899 (1991).
  4. Bergmeyer, H. U. Methods in Enzymatic Analysis 2nd edn (Academic, London, 1974).
  5. Maxwell, I. H., Maxwell, F. & Glode, L. M. Cancer Res. 46, 4660–4664 (1986).
  6. Salmon, D. M. W. & Flatt, J. P. Int. J. Obesity 9, 443–449 (1985).

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Metadata

Authors
Lowell, B. B., S-Susulic, V., Hamann, A., Lawitts, J. A., Himms-Hagen, J., Boyer, B. B., Kozak, L. P., & Flier, J. S.
Affiliations
  • Harvard University (US)
  • University of Alaska Fairbanks (US)
  • Jackson Laboratory (US)
ORCID
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
1993-12
Volume
366
Issue
6457
Pages
740-742
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
DOI
10.1038/366740a0
OpenAlex
W2021760176
Cited by
1,075
References
26
Citations by year
2026: 11 · 2025: 19 · 2024: 20 · 2023: 25 · 2022: 29 · 2021: 36 · 2020: 53 · 2019: 38 · 2018: 54 · 2017: 41 · 2016: 53 · 2015: 52 · 2014: 50 · 2013: 54 · 2012: 39
FWCI
11.33
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Keywords
brown adipose tissue, obesity, transgenic mice, hyperphagia, energy expenditure, nutritional homeostasis, obesity complications
MeSH terms
Uncoupling Protein 1, Animals, Body Weight, Adipose Tissue, Brown, Carrier Proteins, Diphtheria Toxin, Eating, Female, Homeostasis, Ion Channels, Male, Membrane Proteins, Mice, Transgenic, Obesity, Mitochondrial Proteins, Mice

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