title: Antipsychotic drugs and obesity.
abstract: Mechanisms underlying antipsychotic cardiometabolic adverse effects are incompletely understood. This hampers the identification of high-risk patients, low-risk antipsychotics and preventive/ameliorative treatments. Recent clinical, molecular and genetic data suggest that: (i) antipsychotic-naïve samples provide the greatest power for mechanistic studies; (ii) weight and metabolic effects can be discordant, pointing to overlapping and distinct mechanisms; (iii) antipsychotics affect satiety and energy homeostasis signaling; (iv) the specific peptides mediating these effects are unknown but probably overlap with those involved in idiopathic obesity; and (v) single nucleotide polymorphisms in genes encoding known neurotransmitter receptors and metabolic proteins are promising pharmacogenomic targets for countering adverse affects. However, sophisticated molecular studies and genome-wide association studies, ideally in antipsychotic-naïve/first episode samples, are needed to further advance the field.
authors.affiliation: Albert Einstein College of Medicine, Bronx, NY, USA.
authors.forename: Christoph U
authors.initials: CU
authors.lastname: Correll
authors.forename: Todd
authors.initials: T
authors.lastname: Lencz
authors.forename: Anil K
authors.initials: AK
authors.lastname: Malhotra
mesh_terms: D000818:Animals; D014150:Antipsychotic Agents / Q000009:adverse effects* / Q000378:metabolism; D006801:Humans; D009765:Obesity / Q000139:chemically induced* / Q000235:genetics / Q000378:metabolism; D011110:Polymorphism, Genetic; D017981:Receptors, Neurotransmitter / Q000235:genetics / Q000378:metabolism
chemical_list: D014150:Antipsychotic Agents; D017981:Receptors, Neurotransmitter