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Cited by 71Adipose Tissue and MetabolismMetabolism, Diabetes, and CancerPeroxisome Proliferator-Activated Receptors

Role of energy charge and AMP-activated protein kinase in adipocytes in the control of body fat stores

Rossmeisl, M, Flachs, P, Brauner, P, Sponarova, J, Matejkova, O, Prazak, T, Ruzickova, J, Bardova, K +2 more·2004·International Journal of Obesity
DOI 10.1038/sj.ijo.0802855
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Abstract

As indicated by in vitro studies, both lipogenesis and lipolysis in adipocytes depend on the cellular ATP levels. Ectopic expression of mitochondrial uncoupling protein 1 (UCP1) in the white adipose tissue of the aP2-Ucp1 transgenic mice reduced obesity induced by genetic or dietary manipulations. Furthermore, respiratory uncoupling lowered the cellular energy charge in adipocytes, while the synthesis of fatty acids (FA) was inhibited and their oxidation increased. Importantly, the complex metabolic changes triggered by ectopic UCP1 were associated with the activation of AMP-activated protein kinase (AMPK), a metabolic master switch, in adipocytes. Effects of several typical treatments that reduce adiposity, such as administration of leptin, beta-adrenoceptor agonists, bezafibrate, dietary n-3 polyunsaturated FA or fasting, can be compared with a phenotype of the aP2-Ucp1 mice. These situations generally lead to the upregulation of mitochondrial UCPs and suppression of the cellular energy charge and FA synthesis in adipocytes. On the other hand, FA oxidation is increased. Moreover, it has been shown that AMPK in adipocytes can be activated by adipocyte-derived hormones leptin and adiponectin, and also by insulin-sensitizes thiazolidinediones. Thus, it is evident that metabolism of adipose tissue itself is important for the control of body fat content and that the cellular energy charge and AMPK are involved in the control of lipid metabolism in adipocytes. The reciprocal link between synthesis and oxidation of FA in adipocytes represents a prospective target for the new treatment strategies aimed at reducing obesity.

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Crossref · 10.1038/sj.ijo.0802855

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  • In the absence of mechanisms to ensure continuously elevated fuel oxidation, such as those present in brown fat, uncoupling of white adipose tissue mitochondria may decrease ATP levels and impair anabolic flux.

    “These results suggest that, in the absence of mechanisms to ensure continuously elevated fuel oxidation, such as those present in brown fat, uncoupling of white adipose tissue mitochondria may decrease ATP levels and impair anabolic flux (183).”

    From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [183]

  • Gain-of-function studies in mice where ectopic expression of UCPs mitigate diet-induced obesity support the notion that uncoupling could be sufficient.

    “Gain-of-function studies in mice where ectopic expression of UCPs mitigate diet-induced obesity support the notion that uncoupling could be sufficient (183, 184).”

    From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [183]

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Authors
Rossmeisl, M., Flachs, P., Brauner, P., Sponarova, J., Matejkova, O., Prazak, T., Ruzickova, J., Bardova, K., Kuda, O., & Kopecky, J.
Affiliations
Czech Academy of Sciences (CZ)
ORCID
Venue
International Journal of Obesity
Publisher
Springer Science and Business Media LLC
Published
2004-12
Volume
28
Issue
S4
Pages
S38-S44
ISSN
  • 0307-0565 (ISSN-L)
  • 1476-5497
DOI
10.1038/sj.ijo.0802855
OpenAlex
W1985964615
Cited by
71
References
85
Citations by year
2025: 1 · 2024: 1 · 2021: 3 · 2020: 4 · 2019: 2 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 3 · 2014: 6 · 2013: 2 · 2012: 4
FWCI
2.47
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • International Journal of Obesity (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Grantová Agentura České Republiky
  • Akademie Věd České Republiky
Topics
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords
energy charge, AMPK, adipocytes, body fat regulation, UCP1, lipogenesis, lipolysis, fatty acid oxidation, fatty acid synthesis, adipose tissue metabolism, obesity, leptin, adiponectin, thiazolidinediones, insulin sensitization, omega-3 fatty acids, fasting
MeSH terms
Uncoupling Protein 1, Adipose Tissue, Animals, Carrier Proteins, Choristoma, Energy Metabolism, Humans, Ion Channels, Membrane Proteins, Mice, Transgenic, Mitochondria, Models, Biological, Multienzyme Complexes, Obesity, Protein Serine-Threonine Kinases, Adipocytes, Mitochondrial Proteins, Mice, AMP-Activated Protein Kinases

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