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. 2015 Jun 15;5(6):e162. doi: 10.1038/nutd.2015.12

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Copyright © 2015 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Diagram depicting the responses induced by refeeding in control lean and in dietary obese rats. In lean rats, food-derived glucose reaching the hypothalamus is sensed by GLUT2, leading to decreased AMPK and feeding inhibition. This mechanism is disrupted in the obese rats. Although the feeding-induced hypothalamic glucose levels are in excess, the decreased GLUT2 levels impair glucose sensing, leading to inappropriate AMPK increase and abolition of hypophagia.