Cited by 1,630Adipose Tissue and MetabolismMitochondrial Function and PathologyRegulation of Appetite and Obesity

Towards a molecular understanding of adaptive thermogenesis

Lowell, Bradford B., Spiegelman, Bruce M.·2000·Nature

Abstract

Obesity results when energy intake exceeds energy expenditure. Naturally occurring genetic mutations, as well as ablative lesions, have shown that the brain regulates both aspects of energy balance and that abnormalities in energy expenditure contribute to the development of obesity. Energy can be expended by performing work or producing heat (thermogenesis). Adaptive thermogenesis, or the regulated production of heat, is influenced by environmental temperature and diet. Mitochondria, the organelles that convert food to carbon dioxide, water and ATP, are fundamental in mediating effects on energy dissipation. Recently, there have been significant advances in understanding the molecular regulation of energy expenditure in mitochondria and the mechanisms of transcriptional control of mitochondrial genes. Here we explore these developments in relation to classical physiological views of adaptive thermogenesis.

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Crossref · 10.1038/35007527

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96 of 96 references verified0 citation errors · 0 not checkable

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  • Adaptive thermogenesis occurs primarily in the mitochondria of skeletal muscle and brown fat.

    “These latter forms of regulated heat production are referred to as adaptive thermogenesis 3, and occur primarily in the mitochondria of skeletal muscle and brown fat, which are distinct from other body tissues in that their thermogenesis is finely regulated and therefore has the potential to be manipulated therapeutically to serve as a target for obesity treatment.”

    From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [3]

  • The thermogenesis of skeletal muscle and brown fat is finely regulated and has the potential to be manipulated therapeutically as a target for obesity treatment.

    “These latter forms of regulated heat production are referred to as adaptive thermogenesis 3, and occur primarily in the mitochondria of skeletal muscle and brown fat, which are distinct from other body tissues in that their thermogenesis is finely regulated and therefore has the potential to be manipulated therapeutically to serve as a target for obesity treatment.”

    From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [3]

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Authors
Lowell, B. B., & Spiegelman, B. M.
Affiliations
  • Beth Israel Deaconess Medical Center (US)
  • Harvard University (US)
Corresponding author
  • Lowell, Bradford B.
  • Spiegelman, Bruce M.
Venue
Nature
Published
2000-04
Volume
404
Issue
6778
Pages
652-660
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
OpenAlex
W1575263278
Cited by
1,630
References
97
Citations by year
2026: 41 · 2025: 45 · 2024: 47 · 2023: 48 · 2022: 69 · 2021: 70 · 2020: 74 · 2019: 71 · 2018: 84 · 2017: 76 · 2016: 71 · 2015: 77 · 2014: 81 · 2013: 68 · 2012: 67
FWCI
6.75
Type
journal article
Language
en
Open access
closed
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
adaptive thermogenesis, energy expenditure, obesity, mitochondria, mitochondrial transcription, energy balance, ambient temperature, diet
MeSH terms
Uncoupling Protein 1, Adaptation, Physiological, Animals, Body Temperature, Brain, Adipose Tissue, Brown, Carrier Proteins, DNA-Binding Proteins, Energy Metabolism, Food, Forecasting, Gene Expression Regulation, Humans, Ion Channels, Membrane Proteins, Mitochondria, Transcription Factors, Transcription, Genetic, Trans-Activators, Muscle, Skeletal, Mitochondrial Proteins, Nuclear Respiratory Factors, GA-Binding Protein Transcription Factor

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