Abstract | AIM: The occurrence of metabolic syndrome (MS) in schizophrenia patients receiving long-term antipsychotics (APs) contributes to their high mortality rate. We aimed to determine whether genetic polymorphisms of identified candidate genes are associated with MS in our study population. MATERIALS & METHODS: We recruited 206 schizophrenia patients receiving AP treatment for at least a year. Cross-sectional measurements of weight, height, blood pressure, waist and hip circumference, and other lipid profiles were recorded. Patient DNA was genotyped for 16 candidate gene polymorphisms. RESULTS: Of these patients, 59.7% were found to have MS while 40.3% did not. All metabolic parameters were significantly different between the two groups. Only three of the 16 polymorphisms studied showed significant association with MS; rs9939609 of the FTO gene confers risk for MS (odds ratio [OR]: 1.73, 95% CI: 1.07-2.78, p = 0.026), while rs1137101 of the LEPR gene (OR: 0.47, 95% CI: 0.28-0.80, p = 0.005) and rs1801133 of the MTHFR gene (OR: 0.59, 95% CI: 0.35-0.99, p = 0.049) are protective against MS. CONCLUSION: Polymorphisms of the FTO, LEPR and MTHFR genes may play a role in MS in Malaysian schizophrenia patients receiving long-term treatment with APs.
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Authors | Siti Norsyuhada Roffeei, Zahurin Mohamed, Gavin P Reynolds, Mas Ayu Said, Ahmad Hatim, Elsa Haniffah Mejia Mohamed, Syarinaz Ahmad Aida, Nor Zuraida Zainal |
Journal | Pharmacogenomics
(Pharmacogenomics)
Vol. 15
Issue 4
Pg. 477-85
(Mar 2014)
ISSN: 1744-8042 [Electronic] England |
PMID | 24624915
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antipsychotic Agents
- LEPR protein, human
- Proteins
- Receptors, Leptin
- Alpha-Ketoglutarate-Dependent Dioxygenase FTO
- FTO protein, human
- MTHFR protein, human
- Methylenetetrahydrofolate Reductase (NADPH2)
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Topics |
- Adult
- Alpha-Ketoglutarate-Dependent Dioxygenase FTO
- Antipsychotic Agents
(adverse effects, therapeutic use)
- Cross-Sectional Studies
- Female
- Genotype
- Humans
- Male
- Metabolic Syndrome
(chemically induced, genetics)
- Methylenetetrahydrofolate Reductase (NADPH2)
(genetics)
- Polymorphism, Single Nucleotide
(genetics)
- Proteins
(genetics)
- Receptors, Leptin
(genetics)
- Risk
- Schizophrenia
(drug therapy, genetics)
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