ReviewReviews in endocrine & metabolic disorders2022
ATP-consuming futile cycles as energy dissipating mechanisms to counteract obesity.
Review in Reviews in endocrine & metabolic disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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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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Who cites it
44 citing papers in PubMed, 85 citations in OpenAlex.
- Improving incretin-mediated body weight loss via energy expenditure.Trends in endocrinology and metabolism: TEM · 2026Review
- Enhanced metabolic benefits of dietary methionine restriction in cold resistant hybrid UCP1-deficient mice.The Journal of nutritional biochemistry · 2026Article
- ATP synthase is a promising target for identifying activated and non-activated adipose tissues.Nature communications · 2026Article
- Deciphering the Presence of Active Interscapular Brown Adipose Tissue in Humans.Acta physiologica (Oxford, England) · 2026Review
- Chronic cold exposure induces plasticity of mitochondrial calcium uptake in beige and brown fat of UCP1-deficient mice.bioRxiv : the preprint server for biology · 2026Article
- Impact of time-restricted feeding on metabolic health and adipose tissue metabolism in aged female mice with high-fat diet-induced obesity.The Journal of physiology · 2026Article
- IUPHAR review: From foe to friend: Repurposing glucagon to treat obesity and type 2 diabetes.Pharmacological research · 2026Review
- What Do We Know of Human Fuel Use during Aerobic Exercise, and How Do We Know It?Physiology (Bethesda, Md.) · 2026Review
- Adaptive Ketogenic-Mediterranean Protocol (AKMP) in Real Clinical Practice: 14-Week Pre-Post Cohort Study on Glucolipid Markers and Safety.Nutrients · 2025Article
- UCP3 gene variants and obesity in a Pakistani sample population.Scientific reports · 2025Article
- Mitochondrial uncoupling, energy substrate utilization, and brown adipose tissue as therapeutic targets in cancer.npj metabolic health and disease · 2025Review
- The TBLR1/TBL1 Co-Factor Complex Acts as a Transcriptional Checkpoint in the Brown Adipose Tissue Response to Prolonged Cold Exposure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Molecular mechanisms of UCP1-independent thermogenesis: the role of futile cycles in energy dissipation.Journal of physiology and biochemistry · 2025Review
- The metabolically protective energy expenditure increase ofAmerican journal of physiology. Endocrinology and metabolism · 2025Article
- An organism-level quantitative flux model of energy metabolism in mice.Cell metabolism · 2025Article
- Identification of lysosomal lipolysis as an essential noncanonical mediator of adipocyte fasting and cold-induced lipolysis.The Journal of clinical investigation · 2025Article
- Transcriptional dynamics in type 2 diabetes progression is linked with circadian, thermogenic, and cellular stress in human adipose tissue.Communications biology · 2025Article
- Natural bioactive compounds and their mechanisms of action in the management of obesity: a narrative review.Frontiers in nutrition · 2025Review
- Development of an adipocyte differentiation protocol using 3T3-L1 cells for the investigation of the browning process: identification of the PPAR-γ agonist rosiglitazone as a browning reference drug.Frontiers in pharmacology · 2025Article
- Spotlight on the Mechanism of Action of Semaglutide.Current issues in molecular biology · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Obesity results from an imbalance in energy homeostasis, whereby excessive energy intake exceeds caloric expenditure. Energy can be dissipated out of an organism by producing heat (thermogenesis), explaining the long-standing interest in exploiting thermogenic processes to counteract obesity. Mitochondrial uncoupling is a process that expends energy by oxidizing nutrients to produce heat, instead of ATP synthesis. Energy can also be dissipated through mechanisms that do not involve mitochondrial uncoupling. Such mechanisms include futile cycles described as metabolic reactions that consume ATP to produce a product from a substrate but then converting the product back into the original substrate, releasing the energy as heat. Energy dissipation driven by cellular ATP demand can be regulated by adjusting the speed and number of futile cycles. Energy consuming futile cycles that are reviewed here are lipolysis/fatty acid re-esterification cycle, creatine/phosphocreatine cycle, and the SERCA-mediated calcium import and export cycle. Their reliance on ATP emphasizes that mitochondrial oxidative function coupled to ATP synthesis, and not just uncoupling, can play a role in thermogenic energy dissipation. Here, we review ATP consuming futile cycles, the evidence for their function in humans, and their potential employment as a strategy to dissipate energy and counteract obesity.
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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.