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Exercise improves memory loss caused by type 2 diabetes

By Editor
21 December 2016   |   2:23 am
Type 2 diabetes is characterized by impaired glucose metabolism and can cause central nervous system-related complications, such as memory dysfunction.
PHOTO: The Indian Express

PHOTO: The Indian Express

Running actually lowers inflammation in knee joints
Type 2 diabetes is characterized by impaired glucose metabolism and can cause central nervous system-related complications, such as memory dysfunction. The hippocampus is an essential brain component for normal memory formation. However, the effect of impaired glycol-metabolism on hippocampal-mediated memory in type 2 diabetes patients is not known.

In a new study, researchers centered at the University of Tsukaba investigated whether hippocampal glucose metabolism and memory function is altered in a rat model of type 2 diabetes.

The study was published in journal Diabetologia.

Based on the idea that exercise normalizes glycometabolism and improves memory function, the research team also investigated the effects of exercise on hippocampal glycometabolism and memory formation.

Placing the rat in a circular pool and testing its ability to remember the location of a platform that would allow it to escape from the water evaluated Hippocampal function. “This is a well-established method for measuring spatial learning and memory,” study first author Takeru Shima says.

Type 2 diabetic rats needed more time to escape the water and find the platform. However, after four weeks of moderate exercise, they were able to find the platform much faster. “This indicated that exercise significantly improved spatial memory impairments in type 2 diabetic rats,” Shima explains.

Glycogen levels are altered in tissues of diabetes patients, leading to a variety of complications. However, glycogen levels have not yet been investigated in the hippocampus. “We showed for the first time that glycogen levels are significantly higher in the hippocampus of diabetic rats,” corresponding author Hideaki Soya says.

Also, new research from BYU exercise science professors finds that pro-inflammatory molecules actually go down in the knee joint after running.

In other words, it appears running can reduce joint inflammation. “It flies in the face of intuition,” said study coauthor Matt Seeley, associate professor of exercise science at BYU. “This idea that long-distance running is bad for your knees might be a myth.”

In a study recently published in the European Journal of Applied Physiology, Seeley and a group of BYU colleagues, as well as Dr. Eric Robinson from Intermountain Healthcare, measured inflammation markers in the knee joint fluid of several healthy men and women aged 18-35, both before and after running.

The researchers found that the specific markers they were looking for in the extracted synovial fluid—two cytokines named GM-CSF and IL-15—decreased in concentration in the subjects after 30 minutes of running. When the same fluids were extracted before and after a non-running condition, the inflammation markers stayed at similar levels.

“What we now know is that for young, healthy individuals, exercise creates an anti-inflammatory environment that may be beneficial in terms of long-term joint health,” said study lead author Robert Hyldahl, BYU assistant professor of exercise science.

Interestingly, single bout of exercise reduced 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). “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.

Hyldahl said the study results indicate running is chondroprotective, which means exercise may help delay the onset of joint degenerative diseases such as osteoarthritis.

This is potentially great news, since osteoarthritis—the painful disease where cartilage at the end of bones wears down and gradually worsens over time – affects about 27 million people in the United States.

“This study does not indicate that distance runners are any more likely to get osteoarthritis than any other person,” Seeley said. “Instead, this study suggests exercise can be a type of medicine.”

Researchers, which included then undergraduate (and now grad student) Alyssa Evans and PhD student Sunku Kwon, now plan to turn their attention to study subjects with previous knee injuries. Specifically, they’re looking to do similar tests on people who have suffered ACL injuries.

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