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C31H48O5, monoclinic, P21 (no. 4), a = 11.0421(3) Å, b = 6.49710(16) Å, c = 20.4687(4) Å, β = 97.922(2)°, V = 1454.45(6) Å3, Z = 2, Rgt(F) = 0.0382, wRref(F2) = 0.1024, T = 293(2) K.

C7H6BrN5, triclinic, P1̄ (no. 2), a = 8.3319(4) Å, b = 10.0666(5) Å, c = 11.4042(6) Å, α = 107.213(5)°, β = 99.394(4)°, γ = 95.540(4)°, V = 890.71(8) Å3, Z = 4, Rgt(F) = 0.0452, wRref(F2) = 0.0972, T = 293(2) K.

C31H48O5, monoclinic, P21 (no. 4), a = 11.0421(3) Å, b = 6.49710(16) Å, c = 20.4687(4) Å, β = 97.922(2)°, V = 1454.45(6) Å3, Z = 2, Rgt(F) = 0.0382, wRref(F2) = 0.1024, T = 293(2) K. [ABSTRACT FROM AUTHOR]

C7H6BrN5, triclinic, P1̄ (no. 2), a = 8.3319(4) Å, b = 10.0666(5) Å, c = 11.4042(6) Å, α = 107.213(5)°, β = 99.394(4)°, γ = 95.540(4)°, V = 890.71(8) Å3, Z = 4, Rgt(F) = 0.0452, wRref(F2) = 0.0972, T = 293(2) K. [ABSTRACT FROM AUTHOR]

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Objective: To investigate whether there is association between the-2548G/A functional polymorphism in the promoter region of leptin gene and weight gain following antipsychotic agents (APS) acute treatment in schizophrenic patients., Methods: Eight-four Chinese Han untreated schizophrenia patients in 70 nuclear families were recruited. The polymorphism of leptin gene was determined with PCR-RFLP technique. Body weight was measured in the patients on admission the and after 10 weeks treatment with risperidone or chlorpromazine., Results: There was an average (8.00+/-6.13)% increases in baseline weight after the 10 week treatment. There were significant differences in the distribution of allele frequencies (chi2=4.031, P=0.045) between the patients with weight changed >or=7% and <7% subgroups. Family-based association analysis further confirmed the above significant finding by transmission disequilibrium test but not by quantitative trait transmission disequilibrium test., Conclusion: The finding confirms that the-2548G/A polymorphism in promoter region of leptin gene is associated with APS-induced weight gain.

Objective: To investigate whether the -1438G/A polymorphism in the promoter region of 5-HTR2A gene associates with the weight gain following antipsychotic agents (APS) acute treatment in schizophrenic patients., Methods: Eighty-four Chinese Han patients with schizophrenia at the first onset were recruited from among 70 nuclear families. The polymorphism of 5-HTR2A gene was determined with PCR-RFLP technique. Body weight was measured in the patients on admission after 10 weeks of treatment with risperidone or chlorpromazine., Results: There were no statistically significant differences in the distribution frequencies of genotype (chi2: 0.172, v1, P > 0.05) and allele (chi2: 0.121, v1, P > 0.05) of -1438G/A polymorphism of 5-HTR2A gene between subgroups (weight gain >or= 7% or < 7%). Likewise, there was no significant difference in weight gain between genotype groups. By means of transmission disequilibrium test and quantitative transmission disequilibrium test, no significant association between the -1438G/A polymorphism of 5-HTR2A gene and weight gain was observed., Conclusion: 5-HTR2A gene -1438G/A polymorphism was probably not associated with APS-induced weight gain in Chinese Han patients with schizophrenia in this study.

Objective: To investigate whether the -2548G/A functional polymorphism in promoter region of leptin gene influencing weight gain following antipsychotic agents (APS) acute treatment in schizophrenic patients., Methods: 128 Chinese Han untreated patients with schizophrenia (male 61, female 67) with an age and gender matched health controls (n = 38) were recruited. The polymorphism of leptin gene was determined with PCR-RFLP technique. MRI determined abdominal body fat in 22 controls and 30 patients on admission and after 10 weeks treatment with risperidone or chlorpromazine. Body mass index (BMI) was measured on admission and every week subsequently (for patients)., Results: There were average increases in (6.2 +/- 5.7)% of baseline weight and in (38.5 +/- 42)% of baseline abdominal subcutaneous fat (SUB) and in (40.0 +/- 41.2)% of baseline intra-abdominal fat (IAF) 10 weeks after treatment. There were no significant differences in the distribution of allele and genotypes either between the patients and controls or between gender groups. It was found significantly increased weight gain in the patient with the -2548AA genotype (chi(2) = 7.529, df = 1, P = 0.006; OR = 1.941; 95% CI: 1.175 - 3.207); The genotypes had no influence on the baseline weight indicators both in patients and controls. However, as compared with the patients with G allele, the patients with AA genotype had significant increase in BMI (P = 0.003) and SUB (P = 0.009)., Conclusion: The finding identify that the -2548G/A polymorphism in promoter region of leptin gene associated with APS-induced weight gain and abdominal fat deposition and distribution. -2548AA may be a genetic risk factor for the development of weight gain and body fat deposition in Chinese Han schizophrenic patients during APS acute treatment.