Department of Physiology, School of Medicine, Universidad Nacional Autónoma de México (UNAM), PO Box 70250, C.P. 04510 Mexico City, Mexico.
Section of Bioelectronics, Department of Electrical Engineering, Centro de Investigación y Estudios Avanzados del Instituto Politécnico Nacional, PO Box 14740, C.P. 07000 Mexico City, Mexico.
Physiol Behav. 2021 May 15;234:113384. doi: 10.1016/j.physbeh.2021.113384. Epub 2021 Mar 5.
Motor learning skills are reliable indicators of behavioral acquisition and cognitive disorders. The ease with which learning skills are measured disparities the complexity of the interpretation concerning neural plasticity. Conversely, a wealth of information regarding metabolic derangements has long been reported with direct connection to high sucrose diets. However, the impact of excessive sucrose consumption on undergoing cognitive processes has been only scarcely addressed up to now. Therefore, the goal of this work was to describe the associative relationship between high sucrose consumption and changes in motor learning skills acquisition. Motor learning impairments conditioned by central alterations are hypothesized. Rotarod, elevated plus-maze and open field trials, along with metabolic and pro-inflammatory biomarkers tests in Wistar rats under a high sucrose treatment, were performed. Motor learning impairment in high sucrose diet-treated rats was found while spontaneous locomotor activity remained unchanged. Even though, no anxiety-like behavior under high sucrose diet-treatment was observed. Consistently, the worst outcome in the glucose tolerance test was developed, the worst motor learning performance was observed. Furthermore, insulin resistance correlated positively with a pro-inflammatory state and a decreased latency to fall in the rotarod test. Indeed, C-reactive protein and tumor necrosis factor-α serum levels, along with the homeostasis model assessment of insulin resistance (HOMA-IR), significantly increased in motor learning impairment. Together, these results support behavioral, metabolic and pro-inflammatory changes associated with deleterious changes in central nervous system likely involving crucial motor learning structures. Underlying pro-inflammatory-triggered processes may explain cognitive disorders in advanced states of metabolic derangements.
运动学习技能是行为习得和认知障碍的可靠指标。学习技能的测量难度与神经可塑性的解释复杂性形成鲜明对比。相反,长期以来,大量关于代谢紊乱的信息一直与高蔗糖饮食直接相关。然而,到目前为止,还很少有人关注过量蔗糖摄入对认知过程的影响。因此,这项工作的目的是描述高蔗糖消费与运动学习技能获得变化之间的关联关系。假设中枢改变引起的运动学习损伤。在高蔗糖处理下的 Wistar 大鼠中进行了旋转棒、高架十字迷宫和旷场试验,以及代谢和促炎生物标志物测试。发现高蔗糖饮食治疗大鼠的运动学习能力受损,而自发性运动活动保持不变。尽管如此,在高蔗糖饮食治疗下没有观察到类似焦虑的行为。一致的是,葡萄糖耐量试验的结果最差,运动学习表现最差。此外,胰岛素抵抗与促炎状态和旋转棒测试中跌倒潜伏期缩短呈正相关。实际上,C 反应蛋白和肿瘤坏死因子-α血清水平以及胰岛素抵抗的稳态模型评估(HOMA-IR)在运动学习障碍中显著增加。这些结果共同支持与中枢神经系统有害变化相关的行为、代谢和促炎变化,可能涉及关键的运动学习结构。潜在的促炎触发过程可能解释了代谢紊乱晚期的认知障碍。