Using a rat model, researchers from the University of Tsukuba suggest that moderate exercise may help improve the hippocampal memory dysfunction caused by type 2 diabetes.
In their study, published in Diabetologia, the researchers placed the rat in a circular pool and tested its ability to remember the location of a platform that would allow it to escape from the water.
The rats with type 2 diabetes needed more time to escape the water and find the platform. However, after 4 weeks of moderate exercise, they were able to find the platform much faster, according to a media release from University of Tsukuba.
“This indicated that exercise significantly improved spatial memory impairments in type 2 diabetic rats,” explains study first author Takeru Shima, in the release.
“We showed for the first time that glycogen levels are significantly higher in the hippocampus of diabetic rats,” adds corresponding author Hideaki Soya.
A single bout of exercise reduced the rats’ hippocampal glycogen levels, and this correlated with an increase in lactate levels. Lactate is an energy substrate and neuromodulator in the hippocampus, and is known to enhance memory formation. Lactate is transferred to neurons through monocarboxylate transporters (MCTs), the release explains.
“MCT2 expression was significantly lower in the hippocampus of type 2 diabetic rats,” Soya says, “dysregulated MCT2-mediated neuronal uptake of lactate is a possible aetiology of memory dysfunction in type 2 diabetes, and that elevated hippocampal glycogen may be an adaptive change to compensate for the decreased lactate utilization.”
Four weeks of moderate exercise further enhanced glycogen levels and normalized MCT2 expression in the hippocampus of type 2 diabetic rats. These findings suggest that disrupted MCT2-mediated uptake of lactate by neurons contributes to memory dysfunction in type 2 diabetic rats.
The findings indicate that moderate exercise could be used to treat memory impairment in patients with type 2 diabetes by promoting the transfer of glycogen-derived lactate to hippocampal neurons, the release continues.
[Source(s): University of Tsukuba, Science Daily]
