The antipsychotic actions of classic neuroleptics (typical or fi rst-generation antipsychotics, FGA) revolutionized the therapy of schizophrenia, but their extensive use has been impeded by side effects, such as extrapyramidal symptoms, and a high incidence of nonresponders. FGAs, such as haloperidol, act predominantly by blocking dopamine D 2 receptors ( 1 ). Atypical or second-generation antipsychotics (SGA) display relatively weaker antagonism of dopamine D 2 receptors but potent antagonism to serotonin 5-HT 2A receptors ( 1 ). The therapeutic use of SGAs has reduced concern on neurological side effects, but they are not free of metabolically adverse effects. An increase in body weight is fairly rapid after initiating treatment with these drugs. At long term, this may result in overt obesity, along with dyslipidemia, insulin resistance, abnormal glucose tolerance, and diabetes ( 2-4 ). Dyslipidemia is commonly manifested as an increase in total triglyceride and a decrease of high-density lipoprotein (HDL)-cholesterol plasma

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