血浆花生四烯酸水平与双相情感障碍的关系以及 FADS 基因变异的影响。

IF 5.8 1区 医学 Q1 PSYCHIATRY
Takuma Ashizawa, Takeo Saito, Tomo Okochi, Kohei Ninomiya, Kenta Ito, Rei Aoki, Masashi Ikeda, Nakao Iwata
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引用次数: 0

摘要

最近的全基因组关联研究(GWAS)发现,脂肪酸去饱和酶(FADS)基因是双相情感障碍(BD)的易感基因,该基因编码参与多不饱和脂肪酸(PUFA)去饱和的关键酶。多不饱和脂肪酸的一些定量变化表明它们与躁狂症的发病机制有关。因此,本研究旨在通过与 FADS 基因变异(rs174550)相关的脂质组学研究来阐明双相情感障碍与 PUFAs 之间的关系,因为 FADS 基因变异与 PUFA 水平和双相情感障碍易感性相关。利用 BD 组(535 人)和对照组(107 人)的血浆样本测量了 23 种脂肪酸的浓度。比较了两组之间每种 PUFA 浓度比率的差异。此外,还比较了 rs174550 各基因型的 PUFA 浓度比差异。结果显示,BD 组的亚油酸(LA)(β = -0.36,p = 0.023)和花生四烯酸(AA)(β = -0.18,p = 0.013)浓度明显低于对照组。关于 FADS 对 PUFA 浓度比的影响,rs174550 的 C-等位基因携带者的γ-亚麻酸和 AA 浓度比显著降低。之前的一项全球基因组研究报告指出,rs174550的C等位基因会增加BD风险。这一方向与本研究的脂质体结果一致。总之,FADS 和 BD 都被认为能调节 AA 浓度。因此,由于 FADS 基因变异对开展 BD 脂质组学研究至关重要,我们认为必须对 FADS 的等位基因频率进行分析。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Association of plasma arachidonic acid levels with a bipolar disorder and the effects of a FADS gene variant.

Recent genome-wide association studies (GWASs) have identified fatty acid desaturase (FADS) genes, which code key enzymes involved in polyunsaturated fatty acid (PUFA) desaturation as susceptibility genes for bipolar disorder (BD). Several quantitative changes in PUFAs suggest their involvement in BD pathogenesis. Therefore, this study aimed to clarify the relationship between BD and PUFAs by conducting lipidomics covariating with the FADS gene variant (rs174550), which is associated with PUFA levels and BD susceptibility. The concentrations of 23 fatty acids were measured using plasma samples from the BD group (n = 535) and the control group (n = 107). Differences in each PUFA concentration ratio were compared between the two groups. Also, differences in each PUFA concentration ratio were compared for each genotype in rs174550. Our results showed that the BD group had significantly lower concentrations of linoleic acid (LA) (β = -0.36, p = 0.023) and arachidonic acid (AA) (β = -0.18, p = 0.013) than the control group. Concerning the effect of FADS on the PUFA concentration ratio, carriers of C-allele at rs174550 had significantly decreased γ-linolenic acid and AA concentration ratios. A previous GWAS reported that the presence of a C-allele at rs174550 increased the BD risk. This direction is consistent with the lipidomic results of the present study. In conclusion, both the FADS and BD were considered to regulate the AA concentration. Thus, as the FADS gene variant is crucial for conducting lipidomics of BD we believe that the allele frequency of FADS must be analyzed.

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来源期刊
CiteScore
11.50
自引率
2.90%
发文量
484
审稿时长
23 weeks
期刊介绍: Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.
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