Glucose Induces Autophagy Under Starvation Conditions by a P38 MAPK-Dependent Pathway.

Glucose induces autophagy under starvation conditions by a p38 MAPK-dependent pathway.

Filed under: Eating Disorders

Biochem J. 2012 Nov 1;
Moruno-Manchón JF, Pérez-Jiménez E, Knecht E

Autophagy is a natural process of “self-eating” that occurs within cells and can be either pro-survival or can cause cell death. As a pro-survival mechanism, autophagy obtains energy by recycling cellular components such as macromolecules or organelles. In response to nutrient deprivation, e.g. depletion of amino acids or serum, autophagy is induced and most of these signals converge on the kinase mTOR. It is commonly accepted that glucose inhibits autophagy, since its deprivation from cells cultured in full medium induces autophagy by a mechanism involving AMPK, mTOR and Ulk1. However, we show here that under starvation conditions addition of glucose produces the opposite effect. Specifically, our results demonstrate that the presence of glucose induces an increase in the levels of LC3-II, in the number and volume density of autophagic vacuoles and in protein degradation by autophagy. Addition of glucose also increases intracellular ATP, which is in turn necessary for the induction of autophagy because the glycolysis inhibitor oxamate inhibits it, and there is also a good correlation between LC3-II and ATP levels. Moreover, we also show that, surprisingly, the induction of autophagy by glucose is independent of AMPK and mTOR and mainly relies on p38 MAPK.
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