2004 Fiscal Year Final Research Report Summary
A search for glucose intolerance related gene associated with atypical antipsychotics-induced adverse effects
| Project/Area Number |
15591214
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Niigata University |
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Principal Investigator |
SOMEYA Toshiyuki Niigata University, Graduate School of Medical and Dental Sciences, Professor, 大学院・医歯学総合研究科, 教授 (50187902)
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| Co-Investigator(Kenkyū-buntansha) |
MURATAKE Tatsuyuki Niigata University, Medical and Dental Hospital, Lecturer, 医歯学総合病院, 講師 (60311669)
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| Project Period (FY) |
2003 – 2004
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| Keywords | schizophrenia / atypical antipsychotics / glucose intolerance / obesity / genetic vulnerability |
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| Research Abstract |
Recently atypical antipsychotics are widely used for treatment of schizophrenia. Although it is well known that these drugs frequently induce adverse effects, such as glucose intolerance, hyperlipidemia, and obesity, the mechanism of these adverse effects has not been clearly elucidated.
In this study, we investigated the relationship between these side effects and genetic markers in schizophrenic patients treated with atypical antipsychotics, olanzapine or perospirone, in order to develop how to predict these adverse effects in schizophrenic patients with olanzapine and perospirone.
So far, we have collected blood samples and clinical data from 50 schizophrenic patients. We have analyzed the association between side effects such as glucose intolerance, obesity and genetic marker such as dopamine D2 receptor polymorphisms (Taq1A,-141 Ins/Del), beta2 adrenergic receptor polymorphisms (Arg16Gly,Gln27Glu), and beta3 adrenergic receptor polymorphism (Trp64Arg).
A patient, who developed diabetes mellitus during the treatment with perospirone and showed absence of Gly16 mutated allele on beta2 adrenergic receptor which has been regarded as decreasing the risk of diabetes.
Also there was a patient who developed extremely remarkable weight gain while he was treated with olanzapine. The cause is unknown at this point, but it is considered very important to explore the causal genetic factor in such a patient.
Further studies involving larger patient numbers and systematic pharmacogenomic analyses are worthwhile to obtain clinically useful genetic background, with regard to glucose intolerance, hyperlipidemia, and obesity.
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