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代谢综合征中的亚临床血管疾病与脑谷氨酸升高。

Subclinical vascular disease and cerebral glutamate elevation in metabolic syndrome.

机构信息

Department of Psychology, The University of Texas at Austin, 1 University Station, A8000, Austin, TX, 78712, USA.

出版信息

Metab Brain Dis. 2012 Dec;27(4):513-20. doi: 10.1007/s11011-012-9306-x. Epub 2012 May 3.

DOI:10.1007/s11011-012-9306-x
PMID:22552897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3614081/
Abstract

Metabolic syndrome (MetS), the co-occurrence of obesity, hypertension, hyperglycemia and dyslipidema, is an important risk factor for diabetes, cardiovascular disease and end-organ damage in the brain. Our goal was to determine if metabolic syndrome (MetS) differentially affects cerebral metabolism in middle-aged adults with varying degrees of subclinical vascular disease. Sixty-five neurologically healthy adults aged 40 to 60 years (19 with MetS and 46 controls) underwent ultrasound examination of carotid artery intima-media thickness (IMT), a measure of peripheral vascular disease, a full neuropsychological evaluation, and a proton magnetic resonance spectroscopy ((1)H MRS) scan of occipitoparietal grey matter. The Johnson-Neyman technique and pick-a-point approach were used to test if MetS-related neurochemical changes were moderated by IMT. The MetS and control groups were comparable in age, education, gender distribution, average IMT, and cognitive performance. MetS individuals with low IMT values (1 SD below sample mean) demonstrated comparable neurochemical concentrations to the healthy controls (t = -0.21, p = 0.84, 95 % CI -0.106 to 0.086), while MetS individuals with high IMT values (1 SD above sample mean) exhibited significantly elevated glutamate concentrations (t = 2.84, p = 0.006, 95 % CI 0.038 to 0.220). We found that the level of peripheral atherosclerosis moderated the level of elevation of cerebral glutamate concentrations in patients with MetS. These results suggest that peripheral metabolic dysfunction in midlife likely acts in conjunction with subclinical vascular disease to foster pro-neurotoxic conditions in the central nervous system creating early brain vulnerability.

摘要

代谢综合征(MetS)是肥胖、高血压、高血糖和血脂异常的共同发生,是糖尿病、心血管疾病和脑器官损伤的重要危险因素。我们的目标是确定代谢综合征(MetS)是否会对不同程度亚临床血管疾病的中年成年人的大脑代谢产生不同影响。65 名神经健康的 40 至 60 岁成年人(19 名患有 MetS,46 名对照)接受了颈动脉内膜中层厚度(IMT)的超声检查,这是一种外周血管疾病的测量方法,还接受了全面的神经心理学评估和枕顶灰质质子磁共振波谱(1H MRS)扫描。使用 Johnson-Neyman 技术和 pick-a-point 方法来测试 MetS 相关神经化学变化是否受 IMT 调节。MetS 组和对照组在年龄、教育程度、性别分布、平均 IMT 和认知表现方面相当。IMT 值较低(低于样本平均值 1 个标准差)的 MetS 个体与健康对照组的神经化学浓度相当(t=-0.21,p=0.84,95%CI-0.106 至 0.086),而 IMT 值较高(高于样本平均值 1 个标准差)的 MetS 个体则表现出明显升高的谷氨酸浓度(t=2.84,p=0.006,95%CI0.038 至 0.220)。我们发现,外周动脉粥样硬化的程度调节了 MetS 患者大脑谷氨酸浓度升高的程度。这些结果表明,中年时期的外周代谢功能障碍可能与亚临床血管疾病一起作用,在中枢神经系统中产生促神经毒性条件,从而导致早期大脑易损性。

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