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首页> 外文期刊>Pharmacogenomics >Association of HTR2C, but not LEP or INSIG2, genes with antipsychotic-induced weight gain in a German sample.
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Association of HTR2C, but not LEP or INSIG2, genes with antipsychotic-induced weight gain in a German sample.

机译：在德国样本中，HTR2C（而非LEP或INSIG2）与抗精神病药物引起的体重增加相关。

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BACKGROUND: Drug-induced bodyweight gain (BWG) is a serious concern in pharmacotherapy with second-generation antipsychotics. The interindividual variability is likely to be modulated by genetic factors. In the past, pharmacogenetic studies yielded conflicting results, and none of the identified genetic alterations exerts sufficient predictive value for this severe side effect of psychopharmacotherapy. AIM: We aimed to contribute to the replication and extension of prior association findings and investigated the genes encoding serotonin 2C receptor (HTR2C), insulin-induced gene 2 (INSIG2) and leptin (LEP). PATIENTS & METHODS: We investigated the association of HTR2C, LEP and INSIG2 SNPs with antipsychotic-induced BWG in 128 German schizophrenic patients. Genotyping was performed for nine SNPs (HTR2C: rs498207, rs3813928, rs6318 and rs3813929; INSIG2: rs17587100, rs10490624, rs17047764 and rs7566605; LEP: rs7799039). Association analysis included logistic regression analysis and Pearson s chi(2) tests. RESULTS: We report a significant association of three HTR2C SNPs (rs498207, rs3813928 and rs3813929) and of the respective haplotype with antipsychotic-induced BWG. Regarding the X-chromosomal SNP rs498207, individuals with AA/A genotype gained more weight than those with GG/G genotype. The association observed with the SNP rs498207 was also significant after correcting for multiple testing (p = 0.0196). No association was found for INSIG2 and LEP SNPs. CONCLUSION: The results contribute to the accumulating evidence for an association of the X-chromosomal HTR2C gene with antipsychotic-induced BWG. The proposed underlying mechanisms include decreased HTR2C gene expression with reduced 5-HT-modulated activation of hypothalamic proopiomelanocortin-neurons, and inverse 5-HT(2C) agonism in the presence of D(2) receptor antagonism.
机译：背景：在第二代抗精神病药的药物治疗中，药物引起的体重增加（BWG）是一个严重的问题。个体间的变异性很可能受到遗传因素的调节。过去，药物遗传学研究得出相互矛盾的结果，而且没有发现的遗传改变对这种心理药物疗法的严重副作用具有足够的预测价值。目的：我们旨在促进先前关联发现的复制和扩展，并研究了编码5-羟色胺2C受体（HTR2C），胰岛素诱导基因2（INSIG2）和瘦素（LEP）的基因。病人与方法：我们调查了128例德国精神分裂症患者中HTR2C，LEP和INSIG2 SNP与抗精神病药诱发的BWG的关系。对9个SNP进行基因分型（HTR2C：rs498207，rs3813928，rs6318和rs3813929; INSIG2：rs17587100，rs10490624，rs17047764和rs7566605; LEP：rs7799039）。关联分析包括逻辑回归分析和Pearson的chi（2）检验。结果：我们报告三个HTR2C SNPs（rs498207，rs3813928和rs3813929）和各自的单倍型与抗精神病药诱导的BWG显着相关。关于X染色体SNP rs498207，AA / A基因型的个体比GG / G基因型的个体体重增加。校正多次测试后，与SNP rs498207的关联也很显着（p = 0.0196）。找不到INSIG2和LEP SNP的关联。结论：该结果为X-染色体HTR2C基因与抗精神病药诱导的BWG相关的积累证据提供了证据。提出的潜在机制包括降低HTR2C基因表达，降低5-HT调节的下丘脑proopiomelanocortin神经元的激活，以及在存在D（2）受体拮抗作用下反向5-HT（2C）激动。

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