↓ Skip to main content

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

Overview of attention for article published in Genes & Nutrition, December 2011
Altmetric Badge

About this Attention Score

  • Average Attention Score compared to outputs of the same age
  • Above-average Attention Score compared to outputs of the same age and source (57th percentile)

Mentioned by

twitter
1 tweeter

Citations

dimensions_citation
24 Dimensions

Readers on

mendeley
43 Mendeley
Title
Augmenting energy expenditure by mitochondrial uncoupling: a role of AMP-activated protein kinase
Published in
Genes & Nutrition, December 2011
DOI 10.1007/s12263-011-0260-8
Pubmed ID
Authors

Susanne Klaus, Susanne Keipert, Martin Rossmeisl, Jan Kopecky

Abstract

Strategies to prevent and treat obesity aim to decrease energy intake and/or increase energy expenditure. Regarding the increase of energy expenditure, two key intracellular targets may be considered (1) mitochondrial oxidative phosphorylation, the major site of ATP production, and (2) AMP-activated protein kinase (AMPK), the master regulator of cellular energy homeostasis. Experiments performed mainly in transgenic mice revealed a possibility to ameliorate obesity and associated disorders by mitochondrial uncoupling in metabolically relevant tissues, especially in white adipose tissue (WAT), skeletal muscle (SM), and liver. 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. In addition to expected increases in energy expenditure, surprisingly complex phenotypic effects were detected. 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. Experimental data support the idea that (1) while being always activated in response to mitochondrial uncoupling and compromised intracellular energy status in general, AMPK could augment energy expenditure and mediate local as well as whole-body effects; and (2) activation of AMPK alone does not lead to induction of energy expenditure and weight reduction.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 43 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 2%
Czechia 1 2%
Unknown 41 95%

Demographic breakdown

Readers by professional status Count As %
Researcher 11 26%
Student > Bachelor 6 14%
Unspecified 6 14%
Student > Ph. D. Student 6 14%
Professor > Associate Professor 4 9%
Other 10 23%
Readers by discipline Count As %
Agricultural and Biological Sciences 19 44%
Unspecified 8 19%
Biochemistry, Genetics and Molecular Biology 7 16%
Medicine and Dentistry 4 9%
Chemistry 2 5%
Other 3 7%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 06 December 2011.
All research outputs
#2,328,586
of 4,506,051 outputs
Outputs from Genes & Nutrition
#97
of 190 outputs
Outputs of similar age
#99,747
of 231,548 outputs
Outputs of similar age from Genes & Nutrition
#3
of 7 outputs
Altmetric has tracked 4,506,051 research outputs across all sources so far. This one is in the 34th percentile – i.e., 34% of other outputs scored the same or lower than it.
So far Altmetric has tracked 190 research outputs from this source. They receive a mean Attention Score of 2.6. This one is in the 35th percentile – i.e., 35% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 231,548 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 41st percentile – i.e., 41% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 7 others from the same source and published within six weeks on either side of this one. This one has scored higher than 4 of them.