Coupling nutrient sensing to metabolic homoeostasis: the role of the mammalian target of rapamycin complex 1 pathway.

Caroline André, Daniela Cota
Proc. Nutr. Soc.. 2012-08-09; 71(04): 502-510
DOI: 10.1017/s0029665112000754

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1. Proc Nutr Soc. 2012 Nov;71(4):502-10. doi: 10.1017/S0029665112000754. Epub 2012
Aug 9.

Coupling nutrient sensing to metabolic homoeostasis: the role of the mammalian
target of rapamycin complex 1 pathway.

André C(1), Cota D.

Author information:
(1)Group Energy Balance and Obesity, INSERM, Neurocentre Magendie,
Physiophatologie de la Plasticité Neuronale, U862, F-33000 Bordeaux, France.

The mammalian target of rapamycin complex 1 (mTORC1) pathway is known to couple
different environmental cues to the regulation of several energy-demanding
functions within the cell, spanning from protein translation to mitochondrial
activity. As a result, at the organism level, mTORC1 activity affects energy
balance and general metabolic homoeostasis by modulating both the activity of
neuronal populations that play key roles in the control of food intake and body
weight, as well as by determining storage and use of fuel substrates in
peripheral tissues. This review focuses on recent advances made in understanding
the role of the mTORC1 pathway in the regulation of energy balance. More
particularly, it aims at providing an overview of the status of knowledge
regarding the mechanisms underlying the ability of certain amino acids, glucose
and fatty acids, to affect mTORC1 activity and in turn illustrates how the mTORC1
pathway couples nutrient sensing to the hypothalamic regulation of the organisms’
energy homoeostasis and to the control of intracellular metabolic processes, such
as glucose uptake, protein and lipid biosynthesis. The evidence reviewed
pinpoints the mTORC1 pathway as an integrator of the actions of nutrients on
metabolic health and provides insight into the relevance of this intracellular
pathway as a potential target for the therapy of metabolic diseases such as
obesity and type-2 diabetes.

DOI: 10.1017/S0029665112000754
PMID: 22877732 [Indexed for MEDLINE]


Auteurs Bordeaux Neurocampus