mTORC1 in energy expenditure: consequences for obesity

Camille Allard, Cristina Miralpeix, Antonio J. López-Gambero, Daniela Cota
Nat Rev Endocrinol. 2024-01-15; :
DOI: 10.1038/s41574-023-00934-0

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Allard C(#)(1), Miralpeix C(#)(1), López-Gambero AJ(#)(1), Cota D(2).

Author information:
(1) University of Bordeaux, INSERM, Neurocentre Magendie, Bordeaux, France.
(2) University of Bordeaux, INSERM, Neurocentre Magendie, Bordeaux, France.
(#) Contributed equally

In eukaryotic cells, the mammalian target of rapamycin complex 1 (sometimes
referred to as the mechanistic target of rapamycin complex 1; mTORC1)
orchestrates cellular metabolism in response to environmental energy
availability. As a result, at the organismal level, mTORC1 signalling regulates
the intake, storage and use of energy by acting as a hub for the actions of
nutrients and hormones, such as leptin and insulin, in different cell types. It
is therefore unsurprising that deregulated mTORC1 signalling is associated with
obesity. Strategies that increase energy expenditure offer therapeutic promise
for the treatment of obesity. Here we review current evidence illustrating the
critical role of mTORC1 signalling in the regulation of energy expenditure and
adaptive thermogenesis through its various effects in neuronal circuits, adipose
tissue and skeletal muscle. Understanding how mTORC1 signalling in one organ and
cell type affects responses in other organs and cell types could be key to
developing better, safer treatments targeting this pathway in obesity.

© 2024. Springer Nature Limited.

Auteurs Bordeaux Neurocampus