ArticleGenes & nutrition2012
Augmenting energy expenditure by mitochondrial uncoupling: a role of AMP-activated protein kinase.
Article in Genes & nutrition, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Short-term supplementation with a specific combination of dietary polyphenols increases energy expenditure and alters substrate metabolism in overweight subjects.International journal of obesity (2005) · 2014Trial
- Toward a gut-AMPK axis: the microbiome and AMPK signaling in nutrition and healthy aging.Frontiers in physiology · 2026Review
- Understanding metabolic resilience by unraveling temporal dynamics of cellular responses.Trends in endocrinology and metabolism: TEM · 2025Review
- A Mixture ofNutrients · 2024Article
- Water Consumption: Effect on Energy Expenditure and Body Weight Management.Current obesity reports · 2023Review
- A Botanical Mixture Consisting ofNutrients · 2022Article
- Mitochondrial Uncoupling Proteins (UCPs) as Key Modulators of ROS Homeostasis: A Crosstalk between Diabesity and Male Infertility?Antioxidants (Basel, Switzerland) · 2021Review
- The Role of Mitochondrial Adaptation and Metabolic Flexibility in the Pathophysiology of Obesity and Insulin Resistance: an Updated Overview.Current obesity reports · 2021Review
- Neuroprotective Potential of Mild Uncoupling in Mitochondria. Pros and Cons.Brain sciences · 2021Review
- Targeting the Inositol Pyrophosphate Biosynthetic Enzymes in Metabolic Diseases.Molecules (Basel, Switzerland) · 2020Review
- Enhanced Blood Supply Through Lower Body Negative Pressure During Slow-Paced, High Load Leg Press Exercise Alters the Response of Muscle AMPK and Circulating Angiogenic Factors.Frontiers in physiology · 2020Article
- Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases.Cells · 2019Review
- UCP2 expression is associated with weight loss after hypocaloric diet intervention.European journal of clinical nutrition · 2017Article
- Adipocyte-specific deletion of Ip6k1 reduces diet-induced obesity by enhancing AMPK-mediated thermogenesis.The Journal of clinical investigation · 2016Article
- UCP1 and UCP3 Expression Is Associated with Lipid and Carbohydrate Oxidation and Body Composition.PloS one · 2016Article
- Mitochondrial uncoupling proteins and energy metabolism.Frontiers in physiology · 2015Review
- Thiamine deficiency induces anorexia by inhibiting hypothalamic AMPK.Neuroscience · 2014Article
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- Novel aspects of brown adipose tissue biology.Endocrinology and metabolism clinics of North America · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.