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GWAS Study

Genome-wide association study implicates lipid pathway dysfunction in antipsychotic-induced weight gain: multi-ancestry validation.

Liao Y, Yu H, Zhang Y et al.

38336841 PubMed ID
GWAS Study Type
1936 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

LY
Liao Y
YH
Yu H
ZY
Zhang Y
LZ
Lu Z
SY
Sun Y
GL
Guo L
GJ
Guo J
KZ
Kang Z
FX
Feng X
SY
Sun Y
WG
Wang G
SZ
Su Z
LT
Lu T
YY
Yang Y
LW
Li W
LL
Lv L
YH
Yan H
ZD
Zhang D
YW
Yue W
Chapter II

Abstract

Summary of the research findings

Antipsychotic-induced weight gain (AIWG) is a common side effect of antipsychotic medication and may contribute to diabetes and coronary heart disease. To expand the unclear genetic mechanism underlying AIWG, we conducted a two-stage genome-wide association study in Han Chinese patients with schizophrenia. The study included a discovery cohort of 1936 patients and a validation cohort of 534 patients, with an additional 630 multi-ancestry patients from the CATIE study for external validation. We applied Mendelian randomization (MR) analysis to investigate the relationship between AIWG and antipsychotic-induced lipid changes. Our results identified two novel genome-wide significant loci associated with AIWG: rs10422861 in PEPD (P = 1.373 × 10-9) and rs3824417 in PTPRD (P = 3.348 × 10-9) in Chinese Han samples. The association of rs10422861 was validated in the European samples. Fine-mapping and functional annotation revealed that PEPD and PTPRD are potentially causal genes for AIWG, with their proteins being prospective therapeutic targets. Colocalization analysis suggested that AIWG and type 2 diabetes (T2D) shared a causal variant in PEPD. Polygenic risk scores (PRSs) for AIWG and T2D significantly predicted AIWG in multi-ancestry samples. Furthermore, MR revealed a risky causal effect of genetically predicted changes in low-density lipoprotein cholesterol (P = 7.58 × 10-4) and triglycerides (P = 2.06 × 10-3) caused by acute-phase of antipsychotic treatment on AIWG, which had not been previously reported. Our model, incorporating antipsychotic-induced lipid changes, PRSs, and clinical predictors, significantly predicted BMI percentage change after 6-month antipsychotic treatment (AUC = 0.79, R2 = 0.332). Our results highlight that the mechanism of AIWG involves lipid pathway dysfunction and may share a genetic basis with T2D through PEPD. Overall, this study provides new insights into the pathogenesis of AIWG and contributes to personalized treatment of schizophrenia.

1,936 Han Chinese ancestry individuals

Chapter III

Study Statistics

Key metrics and study information

1936
Total Participants
GWAS
Study Type
Yes
Replicated
534 Han Chinese ancestry individuals, 347 European ancestry individuals, 267 African ancestry individuals, 16 individuals
Replication Participants
East Asian, European, African unspecified
Ancestry
China, U.S.
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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