From the Department of Radiology, Shengjing Hospital of China Medical University, Shenyang, PR China.
AJNR Am J Neuroradiol. 2018 Mar;39(3):569-576. doi: 10.3174/ajnr.A5505. Epub 2018 Jan 11.
The neonatal brain has active energy metabolism, and glucose oxidation is the major energy source of brain tissue. Lactate is produced by astrocytes and released to neurons. In the central nervous system, lactate is transported between neurons and astrocytes via the astrocyte-neuron lactate shuttle. The aim of this study was to investigate the regulatory mechanisms of energy metabolism in neurons and astrocytes in the basal ganglia of a neonatal hypoxic-ischemic brain injury piglet model.
A total of 35 healthy piglets (3-5 days of age; 1.0-1.5 kg) were assigned to a control group ( = 5) or a hypoxic-ischemic model group ( = 30). The hypoxic-ischemic model group was further divided into 6 groups according to the H-MR spectroscopy and PET/CT scan times after hypoxia-ischemia (0-2, 2-6, 6-12, 12-24, 24-48, and 48-72 hours; = 5/group). H-MR spectroscopy data were processed with LCModel software. Maximum standard uptake values refer to the maximum standard uptake values for glucose (or FDG). The maximum standard uptake values of the basal ganglia-to-occipital cortex ratio were analyzed. The expression levels of glucose transporters and monocarboxylate transporters were detected by immunohistochemical analysis.
Lactate levels decreased after an initial increase, with the maximal level occurring around 2-6 hours following hypoxia-ischemia. After hypoxia-ischemia, the maximum standard uptake values of the basal ganglia and basal ganglia/occipital cortex initially increased then decreased, with the maximum occurring at approximately 6-12 hours. The lactate and glucose uptake (basal ganglia/occipital cortex maximum standard uptake values) levels were positively correlated. The expression levels of glucose transporter-1 and glucose transporter-3 were positively correlated with the basal ganglia/occipital cortex. The expression levels of monocarboxylic acid transporter-2 and monocarboxylic acid transporter-4 were positively correlated with lactate content.
The results indicate that lactate and glucose transporters have a synergistic effect on the energy metabolism of neurons and astrocytes following hypoxic-ischemic reperfusion brain injury.
新生儿的大脑具有活跃的能量代谢，葡萄糖氧化是脑组织的主要能量来源。乳酸由星形胶质细胞产生并释放到神经元中。在中枢神经系统中，乳酸通过星形胶质细胞-神经元乳酸穿梭在神经元和星形胶质细胞之间运输。本研究旨在探讨新生缺氧缺血性脑损伤猪模型基底节神经元和星形胶质细胞能量代谢的调节机制。
共 35 只健康仔猪（3-5 日龄；1.0-1.5kg）分为对照组（n=5）和缺氧缺血模型组（n=30）。缺氧缺血模型组根据缺氧缺血后 H-MR 光谱和 PET/CT 扫描时间进一步分为 6 组（0-2、2-6、6-12、12-24、24-48 和 48-72 小时；n=5/组）。采用 LCModel 软件处理 H-MR 光谱数据。最大标准摄取值表示葡萄糖（或 FDG）的最大标准摄取值。分析基底节-枕叶皮质最大标准摄取值比值。采用免疫组化分析检测葡萄糖转运体和单羧酸转运体的表达水平。
缺氧缺血后，乳酸水平先升高后降低，缺氧缺血后 2-6 小时达到最高水平。缺氧缺血后，基底节和基底节/枕叶皮质的最大标准摄取值先升高后降低，约在 6-12 小时达到最大值。乳酸和葡萄糖摄取（基底节/枕叶皮质最大标准摄取值）水平呈正相关。葡萄糖转运体-1 和葡萄糖转运体-3 的表达水平与基底节/枕叶皮质呈正相关。单羧酸转运体-2 和单羧酸转运体-4 的表达水平与乳酸含量呈正相关。
结果表明，乳酸和葡萄糖转运体在缺氧缺血再灌注脑损伤后对神经元和星形胶质细胞的能量代谢具有协同作用。
