Inhibition of mTOR prevents glucotoxicity-mediated increase of SA-beta-gal, p16<sup>INK4a</sup>, and insulin hypersecretion, without restoring electrical features of mouse pancreatic islets.

Contrary to our expectations, the 72 h-exposure of the cells to glucotoxicity does not significantly increase the levels of p16 INK4a immunostaining irrespective of the cellular compartment, although a slight trend towards increase was found at 10 and 33 mM glucose compared to 5 mM glucose (Fig. 2 a−c).

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