Exercise-induced ’browning’ of adipose tissues
Open accessAbstract
Global rates of obesity continue to rise and are necessarily the consequence of a long-term imbalance between energy intake and energy expenditure. This is the result of an expansion of adipose tissue due to both the hypertrophy of existing adipocytes and hyperplasia of adipocyte pre-cursors. Exercise elicits numerous physiological benefits on adipose tissue, which are likely to contribute to the associated cardiometabolic benefits. More recently it has been demonstrated that exercise, through a range of mechanisms, induces a phenotypic switch in adipose tissue from energy storing white adipocytes to thermogenic beige adipocytes. This has generated the hypothesis that the process of adipocyte 'browning' may partially underlie the improved cardiometabolic health in physically active populations. Interestingly, 'browning' also occurs in response to various stressors and could represent an adaptive response. In the context of exercise, it is not clear whether the appearance of beige adipocytes is metabolically beneficial or whether they occur as a transient adaptive process to exercise-induced stresses. The present review discusses the various mechanisms (e.g. fatty acid oxidation during exercise, decreased thermal insulation, stressors and angiogenesis) by which the exercise-induced 'browning' process may occur.
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Induction of beige adipocytes by exercise or functional enhancement of existing brown adipose tissue improves total energy expenditure and insulin sensitivity, contributing to fat and weight loss.
“induction of beige adipocytes by exercise or functional enhancement of existing BAT has shown to improve total energy expenditure and insulin sensitivity, contributing to fat and weight loss [16,17,18,19]”
From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [18]
The Summary reports exercise-induced browning of white adipose tissue in rodents and describes beige adipocytes as capable of increasing energy expenditure. It also says the physiological significance is unclear, exercise-induced browning has not been established in humans, and exercise appears to reduce BAT activity. The paper does not establish that browning or BAT enhancement improves insulin sensitivity or causes fat and weight loss. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIncreased metabolic demands during acute exercise are accomplished through mechanisms mostly mediated by the sympathetic nervous system, including white adipose tissue lipolysis dependent on HSL activation by catecholamines, mobilization of hepatic glycogen stores, and antagonism of insulin's anabolic actions through increased cortisol and growth hormone.
“Increased metabolic demands are accomplished through mechanisms that are mostly mediated by the sympathetic nervous system (SNS), such as lipolysis in WAT dependent on the activation of hormone sensitive lipase (HSL) by catecholamines [18,30], mobilization of hepatic glycogen stores, and antagonism of the anabolic actions of insulin through the increased release of cortisol and growth hormone [31]”
From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [18]
In “Regulation of Adipose Tissue Metabolism During Exercise” (page unavailable), the paper supports exercise-induced adipose lipolysis driven chiefly by epinephrine. But it describes epinephrine as activating ATGL, while attributing HSL phosphorylation to natriuretic peptides—not catecholamines. The hepatic glycogen, cortisol, and growth-hormone clauses are attached to a different citation and are not judged here. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAfter the immediate increase, lipolysis in WAT stabilizes but remains higher than the baseline rate for up to 24 h post-exercise.
“For instance, after the immediate increase, lipolysis in WAT stabilizes but remains higher than the baseline rate for up to 24 h post-exercise [18,240], while the increased BMR may persist for up to 48 h [33].”
Physical exercise promotes the browning of WAT and BAT thermogenesis, possibly to meet the increased demand for fatty acid and glucose oxidation and to prevent the accumulation of energy substrates in the circulation.
“Moreover, physical exercise also promotes the browning of WAT and BAT thermogenesis, possibly in order to meet the increased demand for fatty acid and glucose oxidation and to prevent the accumulation of energy substrates in the circulation 123, 124.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [124]
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Obesity and type 2 diabetes mellitus: connections in epidemiology, pathogenesis, and treatments
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“in response to cold exposure (30), exercise (31), and endocrine signals (32).”
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“For instance, after the immediate increase, lipolysis in WAT stabilizes but remains higher than the baseline rate for up to 24 h post-exercise [18,240], while the increased BMR may persist for up to 48 h [33].”
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Inter‐organ communication: a gatekeeper for metabolic health
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Exercise as a Therapeutic Strategy for Obesity: Central and Peripheral Mechanisms
Zhang, Y., Wang, R., Liu, T., & Wang, R. (2024) · Metabolites · doi:10.3390/metabo14110589 · Cited by 27 · see citing works
- Authors
- Aldiss, P., Betts, J., Sale, C., Pope, M., Budge, H., & Symonds, M. E.
- Affiliations
- University of Nottingham (GB)
- University of Bath (GB)
- Nottingham Trent University (GB)
- Corresponding author
- Symonds, Michael E.
- Venue
- Metabolism
- Publisher
- Elsevier BV
- Published
- 2018-04
- Volume
- 81
- Pages
- 63-70
- ISSN
- 0026-0495 (ISSN-L)
- PMC
- PMC5893183
- OpenAlex
- W2769191713
- Cited by
- 175
- References
- 87
- Citations by year
- 2026: 6 · 2025: 15 · 2024: 26 · 2023: 18 · 2022: 25 · 2021: 19 · 2020: 27 · 2019: 22 · 2018: 16 · 2017: 1
- FWCI
- 2.21
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Metabolism (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Pure (University of Bath) (submittedVersion, cc-by-nc-nd)
- Nottingham ePrints (University of Nottingham) (submittedVersion, cc-by-nc-nd)
- Repository@Nottingham (University of Nottingham) (submittedVersion, cc-by)
- Funders
- British Heart Foundation (FS/15/4/31184/)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- beige adipocytes, white adipocytes, thermogenesis, energy expenditure, obesity, cardiometabolic health, fatty acid oxidation, thermal insulation, angiogenesis, stress response, adipocyte hypertrophy, adipocyte hyperplasia
- MeSH terms
- Adaptation, Physiological, Adipose Tissue, Brown, Humans, Stress, Physiological, Exercise, Neovascularization, Physiologic, Adiposity, Adipose Tissue, White
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.
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