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Cells 2012, 1(3), 372-395; doi:10.3390/cells1030372

Regulation of Autophagy by Glucose in Mammalian Cells

Principe Felipe Research Centre, C/Eduardo Primo Yúfera 3, Valencia 46012, Spain
Center for Biomedical Research on Rare Diseases (CIBERER), Valencia 46012, Spain
Authors to whom correspondence should be addressed.
Received: 7 May 2012 / Revised: 22 June 2012 / Accepted: 13 July 2012 / Published: 27 July 2012
(This article belongs to the Special Issue Autophagy)
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Autophagy is an evolutionarily conserved process that contributes to maintain cell homeostasis. Although it is strongly regulated by many extracellular factors, induction of autophagy is mainly produced by starvation of nutrients. In mammalian cells, the regulation of autophagy by amino acids, and also by the hormone insulin, has been extensively investigated, but knowledge about the effects of other autophagy regulators, including another nutrient, glucose, is more limited. Here we will focus on the signalling pathways by which environmental glucose directly, i.e., independently of insulin and glucagon, regulates autophagy in mammalian cells, but we will also briefly mention some data in yeast. Although glucose deprivation mainly induces autophagy via AMPK activation and the subsequent inhibition of mTORC1, we will also comment other signalling pathways, as well as evidences indicating that, under certain conditions, autophagy can be activated by glucose. A better understanding on how glucose regulates autophagy not only will expand our basic knowledge of this important cell process, but it will be also relevant to understand common human disorders, such as cancer and diabetes, in which glucose levels play an important role.
Keywords: autophagy; regulation; nutrients; energy; glucose; AMPK autophagy; regulation; nutrients; energy; glucose; AMPK

This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Moruno, F.; Pérez-Jiménez, E.; Knecht, E. Regulation of Autophagy by Glucose in Mammalian Cells. Cells 2012, 1, 372-395.

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