Towards a molecular understanding of adaptive thermogenesis
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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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
- 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
- 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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