Augmenting energy expenditure by mitochondrial uncoupling: a role of AMP-activated protein kinase

Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F12%3A00377925" target="_blank" >RIV/67985823:_____/12:00377925 - isvavai.cz</a>
Result on the web
<a href="http://dx.doi.org/10.1007/s12263-011-0260-8" target="_blank" >http://dx.doi.org/10.1007/s12263-011-0260-8</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1007/s12263-011-0260-8" target="_blank" >10.1007/s12263-011-0260-8</a>

Result language
angličtina
Original language name
Augmenting energy expenditure by mitochondrial uncoupling: a role of AMP-activated protein kinase
Original language description
Strategies to prevent and treat obesity aim to decrease energy intake and/or increase energy expenditure. Thus, ectopic expression of brown fat-specific mitochondrial uncoupling protein 1 (UCP1) elicited major metabolic effects both at the cellular/tissue level and at the whole-body level. The consequences of mitochondrial uncoupling in WAT and SM are not identical, showing robust and stable obesity resistance accompanied by improvement of lipid metabolism in the case of ectopic UCP1 in WAT, while preservation of insulin sensitivity in the context of high-fat feeding represents the major outcome of muscle UCP1 expression. These complex responses could be largely explained by tissue-specific activation of AMPK, triggered by a depression of cellular energy charge
Czech name
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Czech description
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Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
FB - Endocrinology, diabetology, metabolism, nutrition
OECD FORD branch
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Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
Z - Vyzkumny zamer (s odkazem do CEZ)

Publication year
2012
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

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