Leino R L, Gerhart D Z, Duelli R, Enerson B E, Drewes L R
Department of Anatomy and Cell Biology, School of Medicine, University of Minnesota, Duluth, MN 55812, USA.
Neurochem Int. 2001 May;38(6):519-27. doi: 10.1016/s0197-0186(00)00102-9.
Monocarboxylate transporter (MCT1) levels in brains of adult Long-Evans rats on a high-fat (ketogenic) diet were investigated using light and electron microscopic immunocytochemical methods. Rats given the ketogenic diet (91% fat and 9% protein) for up to 6 weeks had increased levels of the monocarboxylate transporter MCT1 (and of the glucose transporter GLUT1) in brain endothelial cells and neuropil compared to rats on a standard diet. In ketonemic rats, electron microscopic immunogold methods revealed an 8-fold greater MCT1 labeling in the brain endothelial cells at 4 weeks. Abluminal endothelial membranes were twice as heavily labeled as luminal membranes. In controls, luminal and abluminal labeling was not significantly different. The endothelial cytoplasmic compartment was sparsely labeled (<8% of total endothelial labeling) in all brains. Neuropil MCT1 staining was more intense throughout the brain in ketonemic rats, especially in neuropil of the molecular layer of the cerebellum, as revealed by avidin-biotin immunocytochemistry. This study demonstrates that adult rats retain the capacity to upregulate brain MCT1 levels. Furthermore, their brains react to a diet that increases monocarboxylate levels in the blood by enhancing their capability to take up both monocarboxylates (MCT1 upregulation) and glucose (GLUT1 upregulation). This may have important implications for delivery of fuel to the brain under stressful and pathological conditions, such as epilepsy and GLUT1 deficiency syndrome.
采用光镜和电镜免疫细胞化学方法，研究了高脂（生酮）饮食的成年Long-Evans大鼠大脑中一元羧酸转运体（MCT1）的水平。与标准饮食的大鼠相比，给予生酮饮食（91%脂肪和9%蛋白质）长达6周的大鼠，其脑内皮细胞和神经纤维网中一元羧酸转运体MCT1（以及葡萄糖转运体GLUT1）的水平升高。在酮血症大鼠中，电镜免疫金法显示，4周时脑内皮细胞中的MCT1标记增加了8倍。无腔内皮细胞膜的标记强度是有腔细胞膜的两倍。在对照组中，有腔和无腔标记无显著差异。在所有大脑中，内皮细胞质区室的标记都很稀疏（<内皮细胞总标记的8%）。抗生物素蛋白-生物素免疫细胞化学显示，酮血症大鼠全脑的神经纤维网MCT1染色更强，尤其是小脑分子层的神经纤维网。本研究表明，成年大鼠保留上调脑MCT1水平的能力。此外，它们的大脑对增加血液中一元羧酸水平的饮食作出反应，通过增强摄取一元羧酸（MCT1上调）和葡萄糖（GLUT1上调）的能力。这可能对在应激和病理条件下，如癫痫和GLUT1缺乏综合征时向大脑输送燃料具有重要意义。
