Department of Pediatrics, Division of Neonatology and Developmental Biology and Neonatal Research Center, at the UCLA Children's Discovery and Innovation Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Intellectual and Developmental Disabilities Research Center and Brain Research Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Nutrients. 2024 Jul 21;16(14):2363. doi: 10.3390/nu16142363.
Glucose is the primary energy source for most mammalian cells and its transport is affected by a family of facilitative glucose transporters (GLUTs) encoded by the SLC2 gene. GLUT1 and GLUT3, highly expressed isoforms in the blood-brain barrier and neuronal membranes, respectively, are associated with multiple neurodevelopmental disorders including epilepsy, dyslexia, ADHD, and autism spectrum disorder (ASD). Dietary therapies, such as the ketogenic diet, are widely accepted treatments for patients with the GLUT1 deficiency syndrome, while ameliorating certain symptoms associated with GLUT3 deficiency in animal models. A ketogenic diet, high-fat diet, and calorie/energy restriction during prenatal and postnatal stages can also alter the placental and brain GLUTs expression with long-term consequences on neurobehavior. This review focuses primarily on the role of diet/energy perturbations upon GLUT isoform-mediated emergence of neurodevelopmental and neurodegenerative disorders.
葡萄糖是大多数哺乳动物细胞的主要能量来源,其运输受 SLC2 基因编码的一系列易化葡萄糖转运体(GLUT)的影响。GLUT1 和 GLUT3 分别在血脑屏障和神经元膜中高度表达,与多种神经发育障碍有关,包括癫痫、阅读障碍、注意缺陷多动障碍和自闭症谱系障碍(ASD)。饮食疗法,如生酮饮食,被广泛接受为 GLUT1 缺乏综合征患者的治疗方法,同时改善动物模型中与 GLUT3 缺乏相关的某些症状。在产前和产后阶段,生酮饮食、高脂肪饮食和热量/能量限制也会改变胎盘和大脑 GLUT 的表达,对神经行为产生长期影响。本综述主要关注饮食/能量干扰对 GLUT 同工型介导的神经发育和神经退行性疾病发生的作用。