ATP-consuming futile cycles as energy dissipating mechanisms to counteract obesity.
Brown adipose tissue
Energy expenditure
Futile cycle
Malate aspartate shuttle
Metabolism
Thermogenesis
Journal
Reviews in endocrine & metabolic disorders
ISSN: 1573-2606
Titre abrégé: Rev Endocr Metab Disord
Pays: Germany
ID NLM: 100940588
Informations de publication
Date de publication:
02 2022
02 2022
Historique:
accepted:
24
09
2021
pubmed:
7
11
2021
medline:
15
3
2022
entrez:
6
11
2021
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 34741717
doi: 10.1007/s11154-021-09690-w
pii: 10.1007/s11154-021-09690-w
pmc: PMC8873062
doi:
Substances chimiques
Adenosine Triphosphate
8L70Q75FXE
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
121-131Subventions
Organisme : CURE:Digestive Diseases Research Center
ID : NIDDK P30 41301
Organisme : NIAAA NIH HHS
ID : R01 AA026914
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001881
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK063491
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK099618
Pays : United States
Informations de copyright
© 2021. The Author(s).
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