Abstract
Second-generation antipsychotics (SGAs) are currently the mainstay in the pharmacotherapy of some psychiatric disorders, which have improved the quality of life of millions of patients globally. A broad spectrum of activity and diminished liabilities of extrapyramidal side effects have made SGAs better alternatives compared to first-generation antipsychotics. Nevertheless, they display a complex profile of activity by affecting an array of biological targets and, as a result, are associated with a constellation of metabolic abnormalities such as hyperglycemia, dyslipidemia, weight gain, and cardiovascular problems. The SGAs-induced metabolic syndrome's exact mechanism has remained nebulous, but some evidence points the finger at mTOR signaling. In this viewpoint, we propose potential strategies to prevent or alleviate the SGA-induced metabolic adverse effects by modulating the activity of the leucine sensors, Sestrins.