Evidence map›Paper›PMID 36757449›Full record

Trial reportPsychopharmacology2023

Genetic association of the rs17782313 polymorphism with antipsychotic-induced weight gain.

Korbinian Felix Schreyer, Stefan Leucht, Stephan Heres, Werner Steimer

Open access · hybridFull text readRandomized Controlled TrialMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Psychopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Genetic determinants of antidepressant and antipsychotic drug response.European archives of psychiatry and clinical neuroscience · 2025
    Article
  4. Article
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Korbinian Felix SchreyerDepartment of Clinical Chemistry and Pathobiochemistry, School of Medicine, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany. korbinian.schreyer@tum.de.ORCID http://orcid.org/0000-0001-9473-3958
Stefan LeuchtDepartment of Psychiatry and Psychotherapy, School of Medicine, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.
Stephan Hereskbo-Klinik für Psychiatrie und Psychotherapie Nord - Schwabing, Kölner Platz 1, 80804, Munich, Germany.
Werner SteimerDepartment of Clinical Chemistry and Pathobiochemistry, School of Medicine, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany.
Technical University of Munich · DEMünchen Klinik Schwabing · DE

Funding

Bundesministerium für Bildung und Forschung 01KG0910
6 · The paper itself

Abstract

rationaleWeight gain is a frequent side effect of treatment with SGAs (second-generation antipsychotics) and a leading cause for nonadherence. Several candidate genes have been identified that could influence the amount of AIWG (antipsychotic-induced weight gain). The polymorphism rs17782313 near the MC4R (human melanocortin 4 receptor gene) was strongly associated with obesity in a large scale GWAS (genome wide association study), yet previous studies investigating its impact on AIWG did not lead to a definite conclusion regarding its effect. In particular, they were all relatively short and had a naturalistic design.

objectiveWe therefore examined the influence of the rs17782313 polymorphism on SGA-related weight gain.

methodsParticipants of a multicenter randomized, controlled, double-blind study comparing two treatment strategies in individuals with schizophrenia or schizoaffective disorder were genotyped using a rapid-cycle polymerase chain reaction. Up to 252 individuals completed the first 2 weeks (phase I), 212 the entire 8 weeks (hence 'completers'). Patients received either amisulpride or olanzapine or both consecutively. Thirty-seven had their first episode. Weight gain occurring in different genotypes was statistically compared and confounding factors were adjusted by stepwise multiple linear regression. A correction for multiple testing was included.

resultsWithin 212 'completers', carriers of the C allele had a higher absolute weight gain than those homozygous for the T allele (2.6 kg vs. 1.2 kg), though this observation was not significant (P = 0.063). In the amisulpride subpopulation, this association appeared stronger and reached significance (2.5 kg vs. 0.7 kg, P = 0.043), though failed to remain significant after correction for multiple testing. A stepwise multiple linear regression showed a significant association in both the whole study population (P < 0.001) and the amisulpride subpopulation (P < 0.001).

conclusionOur results indicate that the rs17782313 polymorphism might influence antipsychotic-induced weight gain and therefore confirm some of the earlier conclusions.

Indexed as

Antipsychotic AgentsAmisulprideGenome-Wide Association StudyHumansOlanzapinePolymorphism, Single NucleotideReceptor, Melanocortin, Type 4Weight GainAmisulprideAntipsychotic AgentsMC4R protein, humanOlanzapineReceptor, Melanocortin, Type 4AmisulprideAntipsychotic treatmentHuman melanocortin four receptor gene (MC4R)OlanzapinePharmacogeneticsrs17782313Second generation antipsychoticsWeight gain

Identifiers

PMID36757449
PMCPMC10006246
OpenAlexW4319657058

What Socratic holds

Textfull text, public
LicenceCC BY
measurements read71
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.