Related Experiment Video
Updated: May 30, 2026

Self-Administration of Drugs in Mouse Models of Feeding and Obesity
Published on: June 8, 2021
Genetic interactions in the adrenergic system genes: analysis of antipsychotic-induced weight gain
Vincenzo De Luca1, Renan P Souza, Emanuela Viggiano
1Neurogenetics Section, Centre for Addictions and Mental Health, Toronto, ON, Canada. vincenzo_deluca@camh.net
Unlabelled:
Atypical antipsychotics (AP) have high affinity for many neurotransmitter receptors. Among these receptors, APs are antagonist at α-adrenergic and β-adrenergic receptors, and this pharmacological property has been postulated to be involved in the mechanism of action of these drugs with respect to both clinical response and adverse effects.
Objective:
We tested the hypotheses that AP-induced weight gain is associated with genetic variation in adrenergic receptors and pathway enzymes. We analyzed nine genetic polymorphisms across seven adrenergic genes (ADRA1A, ADRA2A, ADRA2C, ADRB3, DBH, MAOA and COMT).
Methods:
One hundred thirty-nine patients with schizophrenia were prospectively assessed for AP-induced weight gain. The HelixTree software (Golden Helix, Bozeman, MT, USA) was employed to detect differences in genotypic distribution between weight gainer and non-weight gainer groups. Furthermore, for the dopamine β-hydroxylase haplotype, we were able to obtain both the molecular and the statistical phases, analyzing the phenotype considering both phases.
Results:
Weight gain was not associated with any adrenergic gene.
Conclusions:
Our results suggest that genetic polymorphisms in the adrenergic system may not play a major role in AP-induced weight gain; however, adrenergic 2A receptor gene that produced previously the most consistent associations with this phenotype showed a significant interaction with the monoamine oxidase A in weight gainers.
Related Concept Videos
Human Genetics
The complex relationship between genetics and psychology is observable through common biological components such...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Antidepressant Drugs: MAOIs and Other Agents
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu
Adrenergic Agonists: Indirect-Acting Agents
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
Drug Toxicity: Risk factors

