Association of the PPAR-¥ã Gene with Altered Glucose Levels and Psychosis Profile in Schizophrenia Patients Exposed to Antipsychotics
Psychiatry Investigation 2014³â 11±Ç 2È£ p.179 ~ p.185
(Liu Yun-Ru) - Taipei Medical University Office of Research and Development
(Hu Tsung-Ming) - Yuli Veterans Hospital
(Lan Tsuo-Hung) - National Yang Ming University Faculty of Medicine
(Chiu Hsien-Jane) - National Yang Ming University Faculty of Medicine
(Chang Yung-Han) - National Yang Ming University Institute of Public Health and Department of Public Health
(Chen Shuo-Fei) - Yu Da University of Science and Technology Department of Health Care and Social Work
(Yu Yen-Hsin) - Academia Sinica Institute of Molecular Biology
(Chen Cheng-Chung) - Kaohsiung Municipal Kai-Syuan Psychiatric Hospital
(Loh El-Wui) - Kaohsiung Municipal Kai-Syuan Psychiatric Hospital
Abstract
Objective: Metabolic abnormalities, e.g., diabetes, are common among schizophrenia patients. Peroxisome proliferator activated receptor-¥ã (PPAR-¥ã) regulates glucose/lipid metabolisms, and schizophrenia like syndrome may be induced by actions involving retinoid X receptor-¥á/PPAR-¥ã heterodimers. We examined a possible role of the PPAR-¥ã gene in metabolic traits and psychosis profile in schizophrenia patients exposed to antipsychotics.
Methods: Single nucleotide polymorphisms (SNPs) of the PPAR-¥ã gene and a serial of metabolic traits were determined in 394 schizophrenia patients, among which 372 were rated with Positive and Negative Syndrome Scale (PANSS).
Results: SNP-10, -12, -18, -19, -20 and -26 were associated with glycated hemoglobin (HbA1c) whereas SNP-18, -19, -20 and -26 were associated with fasting plasma glucose (FPG). While SNP-23 was associated with triglycerides, no associations were identified between the other SNPs and lipids. Further haplotype analysis demonstrated an association between the PPAR-¥ã gene and psychosis profile.
Conclusion: Our study suggests a role of the PPAR-¥ã gene in altered glucose levels and psychosis profile in schizophrenia patients exposed to antipsychotics. Although the Pro12Ala at exon B has been concerned an essential variant in the development of obesity, the lack of association of the variant with metabolic traits in this study should not be treated as impossibility or a proof of error because other factors, e.g., genes regulated by PPAR-¥ã, may have complicated the development of metabolic abnormalities. Whether the PPAR-¥ã gene modifies the risk of metabolic abnormalities or psychosis, or causes metabolic abnormalities that lead to psychosis, remains to be examined.
Å°¿öµå
Schizophrenia, Psychosis, Glucose, PPAR-¥ã gene
KMID :
1118520140110020179
¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸
µîÀçÀú³Î Á¤º¸
À¯È¿¼º°á°ú(Recomendation)