ArticlePloS one2009
Metabolic flux analysis of mitochondrial uncoupling in 3T3-L1 adipocytes.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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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
19 citing papers in PubMed, 32 citations in OpenAlex.
- Metabolic flux analysis in adipose tissue reprogramming.Immunometabolism (Cobham, Surrey) · 2024Review
- Dynamics of redox signaling in aging via autophagy, inflammation, and senescence.Biogerontology · 2023Review
- On the role of macrophages in the control of adipocyte energy metabolism.Endocrine connections · 2019Review
- Enhanced quantification of metabolic activity for individual adipocytes by label-free FLIM.Scientific reports · 2018Article
- Multiplatform Metabolomics Investigation of Antiadipogenic Effects on 3T3-L1 Adipocytes by a Potent Diarylheptanoid.Journal of proteome research · 2018Article
- MCT1 and MCT4 Expression and Lactate Flux Activity Increase During White and Brown Adipogenesis and Impact Adipocyte Metabolism.Scientific reports · 2017Article
- Regulation of glycolysis in brown adipocytes by HIF-1α.Scientific reports · 2017Article
- Monoethylhexyl Phthalate Elicits an Inflammatory Response in Adipocytes Characterized by Alterations in Lipid and Cytokine Pathways.Environmental health perspectives · 2017Article
- Acetylcholine released by endothelial cells facilitates flow-mediated dilatation.The Journal of physiology · 2016Article
- Mitochondrial metabolites extend lifespan.Aging cell · 2016Article
- Article
- Niclosamide ethanolamine-induced mild mitochondrial uncoupling improves diabetic symptoms in mice.Nature medicine · 2014Article
- Cultured 3T3L1 adipocytes dispose of excess medium glucose as lactate under abundant oxygen availability.Scientific reports · 2014Article
- AMP-activated protein kinase: an emerging drug target to regulate imbalances in lipid and carbohydrate metabolism to treat cardio-metabolic diseases.Journal of lipid research · 2012Review
- Augmenting energy expenditure by mitochondrial uncoupling: a role of AMP-activated protein kinase.Genes & nutrition · 2012Article
- G protein coupled receptor kinase 2 interacting protein 1 (GIT1) is a novel regulator of mitochondrial biogenesis in heart.Journal of molecular and cellular cardiology · 2011Article
- Advanced stoichiometric analysis of metabolic networks of mammalian systems.Critical reviews in biomedical engineering · 2011Review
- Enhanced glycogen metabolism in adipose tissue decreases triglyceride mobilization.American journal of physiology. Endocrinology and metabolism · 2010Article
- FoxO1 interacts with transcription factor EB and differentially regulates mitochondrial uncoupling proteins via autophagy in adipocytes.Cell death discoveryArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIncreasing energy expenditure at the cellular level offers an attractive option to limit adiposity and improve whole body energy balance. In vivo and in vitro observations have correlated mitochondrial uncoupling protein-1 (UCP1) expression with reduced white adipose tissue triglyceride (TG) content. The metabolic basis for this correlation remains unclear. METHODOLOGY/PRINCIPAL
findingsThis study tested the hypothesis that mitochondrial uncoupling requires the cell to compensate for the decreased oxidation phosphorylation efficiency by up-regulating lactate production, thus redirecting carbon flux away from TG synthesis. Metabolic flux analysis was used to characterize the effects of non-lethal, long-term mitochondrial uncoupling (up to 18 days) on the pathways of intermediary metabolism in differentiating 3T3-L1 adipocytes. Uncoupling was induced by forced expression of UCP1 and chemical (FCCP) treatment. Chemical uncoupling significantly decreased TG content by ca. 35%. A reduction in the ATP level suggested diminished oxidative phosphorylation efficiency in the uncoupled adipocytes. Flux analysis estimated significant up-regulation of glycolysis and down-regulation of fatty acid synthesis, with chemical uncoupling exerting quantitatively larger effects. CONCLUSIONS/SIGNIFICANCE: The results of this study support our hypothesis regarding uncoupling-induced redirection of carbon flux into glycolysis and lactate production, and suggest mitochondrial proton translocation as a potential target for controlling adipocyte lipid metabolism.
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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.