Exercise Could Improve Memory in Patients with Diabetes

Recent findings suggest that moderate exercise could potentially improve memory dysfunction in patients with type 2 diabetes. In these patients, increased transportation of lactate to neurons may cause memory dysfunction in the hippocampus.

Impaired glucose metabolism can cause numerous nervous system-related complications, including memory problems. The hippocampus is crucial for normal memory formation, but the effect of suboptimal glucose metabolism on memory in these patients is unknown.

In a new study published by Diabetologia, researchers aimed to determine whether hippocampal glucose metabolism and memory is impaired in rat models of type 2 diabetes. Since exercise normalizes glucose metabolism and improves memory, the authors also analyzed whether it could improve glucose metabolism and memory.

Memory function was evaluated by placing the rat in a pool, and assessing its ability to remember the location of a platform where the rat could remove itself from the water.

"This is a well-established method for measuring spatial learning and memory," said study first author Takeru Shima, a graduate student at the University of Tsukuba.

According to the study, rat models of type 2 diabetes required additional time to find the platform compared with control rats. However, investigators found that rat models of type 2 diabetes found the platform quicker after only 4 weeks of moderate exercise.

"This indicated that exercise significantly improved spatial memory impairments in type 2 diabetic rats," Shima said.

Type 2 diabetes also causes a change in glycogen levels in numerous tissues, which can lead to disease complications, but the effect of glycogen levels in the hippocampus have not been previously established.

“We showed for the first time that glycogen levels are significantly higher in the hippocampus of diabetic rats," said corresponding author Hideaki Soya, PhD.

The researchers found that a single session of moderate exercise reduced hippocampal glycogen levels, and increased lactate levels. Lactate is known to improve memory formation, and is transferred to neurons through monocarboxylate transporters (MCTs).

"MCT2 expression was significantly lower in the hippocampus of type 2 diabetic rats," Soya said. "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."

After 4 weeks of moderate exercise, glycogen levels were further enhanced, and MCT2 expression in the hippocampus was normalized in rat models of type 2 diabetes.

These findings suggest that disrupted MCT2-mediated uptake of lactate by neurons may play a role in memory dysfunction. Additional studies are needed to explore this relationship further, but implementing an exercise regimen in patients with type 2 diabetes will also benefit many other aspects of the patient’s health, the study concluded.