Long-term light and moderate exercise intervention similarly prevent both hippocampal and glycemic dysfunction in presymptomatic type 2 diabetic rats
Long-term light and moderate exercise intervention similarly prevent both hippocampal and glycemic dysfunction in presymptomatic type 2 diabetic rats
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DOI：
10.1152/ajpendo.00326.2021
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发表时间：
2022-03-01
影响因子：
5.1
通讯作者：
Soya, Hideaki
中科院分区：
文献类型：
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作者：
Jesmin, Subrina;Shima, Takeru;Soya, Hideaki
糖尿病前期人群认知能力下降和2型糖尿病（T2 DM）的风险增加。本研究调查了在T2 DM大鼠模型中，从症状前阶段开始进行4个月的运动干预是否可以预防记忆功能障碍和脑糖原代谢失调的进展。以Long-Evans德岛（LETO）大鼠为遗传对照，在T2 DM模型大冢-长-埃文斯-德岛脂肪（OLETF）大鼠的症状前阶段评估记忆功能以及生化和分子特征。这些大鼠进行轻或中等强度的跑台运动4个月，重复相同的实验。在症状前阶段的OLETF大鼠中观察到显著的海马依赖性记忆功能障碍，伴有海马单羧酸转运蛋白2（MCT 2）（一种神经元乳酸转运蛋白）水平下调，而海马糖原水平无变化。从T2 DM症状前期开始进行4个月的轻度或中度运动，通过MCT 2、糖原和脑源性神经营养因子（BDNF）水平使血糖参数和海马分子正常化，并改善OLETF大鼠的记忆功能障碍。一个4个月的运动方案，从前驱阶段的T2 DM在轻，中等强度的预防发展的T2 DM和认知能力下降的进展与海马乳酸转运和BDNF的improvementation.NEW和值得注意的2型糖尿病是一个独立的危险因素海马记忆功能障碍，这将进展自前驱阶段。我们发现，4个月的轻、中等强度的运动可以阻止症状前糖尿病记忆功能障碍的进展，并改善海马MCT 2的表达，这意味着轻强度运动可能是一种治疗方法，海马MCT 2的改变可能是症状前糖尿病记忆功能障碍的治疗靶点。
A prediabetic population has an increased risk of cognitive decline and type 2 diabetes mellitus (T2DM). This study investigated whether the progression of memory dysfunction and dysregulated brain glycogen metabolism is prevented with 4 mo of exercise intervention from the presymptomatic stage in a T2DM rat model. Memory function and biochemical and molecular profiles were assessed in the presymptomatic stage of Otsuka-Long-Evans-Tokushima fatty (OLETF) rats, a T2DM model, with Long-Evans Tokushima (LETO) rats as genetic control. These rats were subjected to light-or moderate-intensity treadmill running for 4 mo with repetition of the same experiments. Significant hippocampal-dependent memory dysfunction was observed in the pre-symptomatic stage of OLETF rats, accompanied by downregulated levels of hippocampal monocarboxylate transporter 2 (MCT2), a neuronal lactate-transporter, without alteration in hippocampal glycogen levels. Four months of light or moderate exercise from the presymptomatic stage of T2DM normalized glycemic parameters and hippocampal molecular normalization through MCT2, glycogen, and brain-derived neurotrophic factor (BDNF) levels with the improvement of memory dysfunction in OLETF rats. A 4-mo exercise regimen from the presymptomatic stage of T2DM at a light and moderate intensities contributed to the prevention of the development of T2DM and the progression of cognitive decline with hippocampal lactate-transport and BDNF improvement.NEW & NOTEWORTHY Type 2 diabetes mellitus is an independent risk factor for hippocampal memory dysfunction, which would progress since the prediabetic stage. We found that 4 mo of exercise both at the light and moderate intensity prevented the progression of memory dysfunction with an improvement of hippocampal MCT2 expression in presymptomatic diabetes, implying that light intensity exercise could be a therapeutic approach, and the alteration of hippocampal MCT2 would be a thera-peutic target of memory dysfunction from presymptomatic diabetes.