Response to the letter: Angiotensin-II induced insulin resistance.

e have examined with attention the comments of the letter to the Editor in regards to our recently published article (1), and want to thank its authors for their interest in our work. Indeed, it has been demonstrated that, upon acting on the AT1 receptor, angio-tensin II activates matrix metalloproteases that release the epidermal growth factor (EGF), binding to its receptor promotes the activation of mammalian target of ra-pamycin (mTOR) and ribosomal S6 kinase-1, both of which inhibit phosphatidylino-sitol 3-kinase insulin signaling, thus favoring insulin resistance (2-4). Interestingly, some clinical studies have demonstrated that treatment with either angiotensin I-con -verter enzyme inhibitors (ACEI) or angiotensin II receptor antagonist (ARA) reduces the incidence of