0377925 - FGÚ 2013 RIV US eng J - Journal Article
Klaus, S. - Keipert, S. - Rossmeisl, Martin - Kopecký, Jan
Augmenting energy expenditure by mitochondrial uncoupling: a role of AMP-activated protein kinase.
Genes and Nutrition. Roč. 7, č. 3 (2012), s. 369-386. ISSN 1555-8932. E-ISSN 1865-3499
R&D Projects: GA MZd(CZ) NS10528; GA MŠMT(CZ) 7E10059; GA MŠMT(CZ) OC08008
Institutional research plan: CEZ:AV0Z50110509
Keywords : adipose tissue * skeletal muscle * uncoupling protein * transgenic mice * insulin sensitivity
Subject RIV: FB - Endocrinology, Diabetology, Metabolism, Nutrition
Impact factor: 3.329, year: 2012 ; AIS: 0.723, rok: 2012
DOI: https://doi.org/10.1007/s12263-011-0260-8

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
Permanent Link: http://hdl.handle.net/11104/0209945