AMP-Activated Protein Kinase (AMPK) Regulates Energy Metabolism through Modulating Thermogenesis in Adipose Tissue
Open accessAbstract
Obesity occurs when excess energy accumulates in white adipose tissue (WAT), whereas brown adipose tissue (BAT), which is specialized in dissipating energy through thermogenesis, potently counteracts obesity. White adipocytes can be converted to thermogenic "brown-like" cells (beige cells; WAT browning) under various stimuli, such as cold exposure. AMP-activated protein kinase (AMPK) is a crucial energy sensor that regulates energy metabolism in multiple tissues. However, the role of AMPK in adipose tissue function, especially in the WAT browning process, is not fully understood. To illuminate the effect of adipocyte AMPK on energy metabolism, we generated Adiponectin-Cre-driven adipose tissue-specific AMPK α1/α2 KO mice (AKO). These AKO mice were cold intolerant and their inguinal WAT displayed impaired mitochondrial integrity and biogenesis, and reduced expression of thermogenic markers upon cold exposure. High-fat-diet (HFD)-fed AKO mice exhibited increased adiposity and exacerbated hepatic steatosis and fibrosis and impaired glucose tolerance and insulin sensitivity. Meanwhile, energy expenditure and oxygen consumption were markedly decreased in the AKO mice both in basal conditions and after stimulation with a β3-adrenergic receptor agonist, CL 316,243. In contrast, we found that in HFD-fed obese mouse model, chronic AMPK activation by A-769662 protected against obesity and related metabolic dysfunction. A-769662 alleviated HFD-induced glucose intolerance and reduced body weight gain and WAT expansion. Notably, A-769662 increased energy expenditure and cold tolerance in HFD-fed mice. A-769662 treatment also induced the browning process in the inguinal fat depot of HFD-fed mice. Likewise, A-769662 enhanced thermogenesis in differentiated inguinal stromal vascular fraction (SVF) cells via AMPK signaling pathway. In summary, a lack of adipocyte AMPKα induced thermogenic impairment and obesity in response to cold and nutrient-overload, respectively, whereas chronic AMPK activation by A-769662 promoted WAT browning in inguinal WAT and protected against HFD-induced obesity and related metabolic dysfunction. These findings reveal a vital role for adipocyte AMPK in regulating the browning process in inguinal WAT and in maintaining energy homeostasis, which suggests that the targeted activation of adipocyte AMPK may be a promising strategy for anti-obesity therapy.
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Increased AMPK activity enhances mitochondrial biogenesis, supporting sustained fat oxidation and muscle preservation under caloric deficit.
“Increased AMPK activity enhances mitochondrial biogenesis, supporting sustained fat oxidation and muscle preservation under caloric deficit [83,84].”
From Beyond Calories: Individual Metabolic and Hormonal Adaptations Driving Variability in Weight Management—A State-of-the-Art Narrative Review (2024) · cites this paper as [83]
AMPK is activated under low energy states, enhancing fat oxidation and reducing reliance on muscle protein for energy.
“Adenosine monophosphate-activated protein kinase (AMPK) is activated under low energy states, enhancing fat oxidation and reducing reliance on muscle protein for energy.”
From Beyond Calories: Individual Metabolic and Hormonal Adaptations Driving Variability in Weight Management—A State-of-the-Art Narrative Review (2024) · cites this paper as [83]
Genetic variations in AMPK subunit genes and epigenetic modifications affecting AMPK expression can influence the extent of this energy shift.
“Genetic variations in AMPK subunit genes (PRKAA1, PRKAA2) and epigenetic modifications affecting AMPK expression can influence the extent of this energy shift.”
From Beyond Calories: Individual Metabolic and Hormonal Adaptations Driving Variability in Weight Management—A State-of-the-Art Narrative Review (2024) · cites this paper as [83]
Individuals with high AMPK activation efficiently switch to fat as a fuel source, preserving muscle mass during restriction.
“Individuals with high AMPK activation efficiently switch to fat as a fuel source, preserving muscle mass during restriction.”
From Beyond Calories: Individual Metabolic and Hormonal Adaptations Driving Variability in Weight Management—A State-of-the-Art Narrative Review (2024) · cites this paper as [83]
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- Authors
- Wu, L., Zhang, L., Li, B., Jiang, H., Duan, Y., Xie, Z., Shuai, L., Li, J., & Li, J.
- Affiliations
- Chinese Academy of Sciences (CN)
- East China Normal University (CN)
- Corresponding author
- Li, Jingya
- Venue
- Frontiers in Physiology
- Publisher
- Frontiers Media SA
- Published
- 2018-02-21
- Volume
- 9
- Pages
- 122-122
- ISSN
- 1664-042X (ISSN-L)
- PMC
- PMC5826329
- OpenAlex
- W2794345887
- Cited by
- 255
- References
- 78
- Citations by year
- 2026: 18 · 2025: 30 · 2024: 29 · 2023: 26 · 2022: 41 · 2021: 45 · 2020: 34 · 2019: 25 · 2018: 7
- FWCI
- 19.08
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Physiology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81673493, 81673489, 2016YFC1305500)
- Ruijin Hospital
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- AMPK, white adipose tissue browning, thermogenesis, obesity, energy metabolism, cold exposure, high-fat diet, A769662, mitochondrial biogenesis, hepatic steatosis, insulin resistance, energy expenditure, beta3-adrenergic receptor
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 ›
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