Research Article

Genetic interactions in the adrenergic system genes: analysis of antipsychotic-induced weight gain

  1. Vincenzo De Luca1,*,
  2. Renan P. Souza1,
  3. Emanuela Viggiano1,
  4. Laertes Sickert1,
  5. Celine Teo1,
  6. Clement Zai1,
  7. Arun K. Tiwari1,
  8. Daniel J Müller1,
  9. Jeffery A. Lieberman2,
  10. Jan Volavka3,
  11. Herbert Y. Meltzer4,
  12. James L. Kennedy1

Article first published online: 8 AUG 2011

DOI: 10.1002/hup.1219

Issue

Human Psychopharmacology: Clinical and Experimental

Human Psychopharmacology: Clinical and Experimental

Volume 26, Issue 6, pages 386–391, August 2011

Additional Information

How to Cite

Luca, V. D., Souza, R. P., Viggiano, E., Sickert, L., Teo, C., Zai, C., Tiwari, A. K., Müller, D. J., Lieberman, J. A., Volavka, J., Meltzer, H. Y. and Kennedy, J. L. (2011), Genetic interactions in the adrenergic system genes: analysis of antipsychotic-induced weight gain. Hum. Psychopharmacol. Clin. Exp., 26: 386–391. doi: 10.1002/hup.1219

Author Information

  1. 1

    Neurogenetics Section, Centre for Addictions and Mental Health, Toronto, ON, Canada

  2. 2

    Department of Psychiatry, Columbia University, NY, USA

  3. 3

    Institute for Psychiatric Research Nathan S. Kline, Orenburg, NY, USA

  4. 4

    Department of Psychiatry, Vanderbilt University, Nashville, TN, USA

*Dr. V. De Luca, Centre for Addiction and Mental Health, 250 College Street, Room 30, Toronto, ON, Canada, M5T 1R8. Tel: +416 535-8501 ext. 4421; Fax: +416 979 4666. E-mail: vincenzo_deluca@camh.net

Publication History

  1. Issue published online: 26 AUG 2011
  2. Article first published online: 8 AUG 2011
  3. Manuscript Accepted: 11 JUN 2011
  4. Manuscript Revised: 30 MAY 2011
  5. Manuscript Received: 5 FEB 2011

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Keywords:

  • adrenoceptors;
  • antipsychotics;
  • genetic polymorphisms;
  • schizophrenia;
  • metabolic syndrome

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. Copyright © 2011 John Wiley & Sons, Ltd.

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