目的:大量研究报道了酒精使用障碍(AUD)患者的广泛脑代谢异常,但是高血压的促动脉粥样硬化条件的影响,2型糖尿病,丙型肝炎血清阳性,和高脂血症对代谢产物水平的影响未被考虑。这些情况与那些没有AUD的人的脑代谢异常有关。我们预测具有AUD和促动脉粥样硬化条件(Atherogenic+)的寻求治疗的个体表现出神经元活力[N-乙酰天冬氨酸(NAA)]和细胞膜更新/合成[含胆碱化合物(Cho)]的较低区域代谢物标记,与AUD无致动脉粥样硬化条件(Atherogenic-)和健康对照(CON)的患者相比。
方法:Atherogenic+(n=59)和Atherogenic-(n=51)和CON(n=49)完成了1.5T质子磁共振波谱成像研究。各组在NAA上进行了比较,Cho,总肌酸,皮质灰质(GM)中的肌醇,白质(WM),并选择皮质下区域。
结果:致动脉粥样硬化+的额叶GM和颞叶WMNAA低于CON。致动脉粥样硬化+显示较低的顶叶GM,额叶,顶叶和枕骨WM和双凸状核NAA水平高于生热和CON。生热-显示正面GM和WMNAA低于CON。在额叶GM中,致动脉粥样硬化+的Cho水平低于CON,顶叶WM,还有丘脑.动脉粥样硬化+显示比动脉粥样硬化和CON更低的额叶WM和小脑VermisCho。
结论:研究结果表明,AUD患者的致动脉粥样硬化疾病与神经元完整性和细胞膜更新/合成的损害增加有关。在动脉粥样硬化+中观察到的更大的代谢物异常可能与神经元和神经胶质细胞结构的氧化应激相关损害增加和/或动脉血管反应性/管腔活力受损有关。
OBJECTIVE: Widespread brain metabolite abnormalities in those with alcohol use disorder (AUD) were reported in numerous studies, but the effects of the pro-atherogenic conditions of hypertension, type 2 diabetes mellitus, hepatitis C seropositivity, and hyperlipidemia on metabolite levels were not considered. These conditions were associated with brain metabolite abnormalities in those without AUD. We predicted treatment-seeking individuals with AUD and pro-atherogenic conditions (Atherogenic+) demonstrate lower regional metabolite markers of neuronal viability [N-acetylaspartate (NAA)] and cell membrane turnover/synthesis [choline-containing compounds (Cho)], compared with those with AUD without pro-atherogenic conditions (Atherogenic-) and healthy controls (CON).
METHODS: Atherogenic+ (n = 59) and Atherogenic- (n = 51) and CON (n = 49) completed a 1.5 T proton magnetic resonance spectroscopic imaging study. Groups were compared on NAA, Cho, total creatine, and myoinositol in cortical gray matter (GM), white matter (WM), and select subcortical regions.
RESULTS: Atherogenic+ had lower frontal GM and temporal WM NAA than CON. Atherogenic+ showed lower parietal GM, frontal, parietal and occipital WM and lenticular nuclei NAA level than Atherogenic- and CON. Atherogenic- showed lower frontal GM and WM NAA than CON. Atherogenic+ had lower Cho level than CON in the frontal GM, parietal WM, and thalamus. Atherogenic+ showed lower frontal WM and cerebellar vermis Cho than Atherogenic- and CON.
CONCLUSIONS: Findings suggest proatherogenic conditions in those with AUD were associated with increased compromise of neuronal integrity and cell membrane turnover/synthesis. The greater metabolite abnormalities observed in Atherogenic+ may relate to increased oxidative stress-related compromise of neuronal and glial cell structure and/or impaired arterial vasoreactivity/lumen viability.