Possible involvement of AMP-activated protein kinase in obesity resistance induced by respiratory uncoupling in white fat
Language English Country Great Britain, England Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
15225642
DOI
10.1016/j.febslet.2004.06.002
PII: S0014579304007124
Knihovny.cz E-resources
- MeSH
- Adenylate Kinase metabolism MeSH
- DNA Primers MeSH
- Epididymis MeSH
- Animals, Genetically Modified MeSH
- Ion Channels MeSH
- Skin MeSH
- Oleic Acid metabolism MeSH
- Membrane Proteins genetics metabolism MeSH
- Mitochondrial Proteins MeSH
- Mice, Inbred C57BL MeSH
- Mice MeSH
- Obesity genetics MeSH
- Oxidation-Reduction MeSH
- Reverse Transcriptase Polymerase Chain Reaction MeSH
- Immunity, Innate genetics MeSH
- Base Sequence MeSH
- Oxygen Consumption MeSH
- Carrier Proteins genetics metabolism MeSH
- Adipose Tissue enzymology physiopathology MeSH
- Uncoupling Protein 1 MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Adenylate Kinase MeSH
- DNA Primers MeSH
- Ion Channels MeSH
- Oleic Acid MeSH
- Membrane Proteins MeSH
- Mitochondrial Proteins MeSH
- Carrier Proteins MeSH
- Ucp1 protein, mouse MeSH Browser
- Uncoupling Protein 1 MeSH
The AMP-activated protein kinase (AMPK) cascade is a sensor of cellular energy charge that promotes catabolic and inhibits anabolic pathways. However, the role of AMPK in adipocytes is poorly understood. We show that transgenic expression of mitochondrial uncoupling protein 1 in white fat, which induces obesity resistance in mice, is associated with depression of cellular energy charge, activation of AMPK, downregulation of adipogenic genes, and increase in lipid oxidation. Activation of AMPK may explain the complex metabolic changes in adipose tissue of these animals and our results support a role for adipocyte AMPK in the regulation of storage of body fat.
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