New research provides insights into the ability of muscles to take in glucose – University of Copenhagen

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26 June 2013

New research provides insights into the ability of muscles to take in glucose

Insulin resistance

New studies conducted by a Danish research group from University of Copenhagen have identified a molecule which can explain why blood sugar regulation functions poorly in patients with type 2 diabetes and why exercise increases the body's ability to take in glucose.


The hormone insulin functions poorly in patients with type 2 diabetes. This is called insulin resistance and means that the muscles have difficulties taking in glucose from the blood.

Insulin resistance linked with Rac1-molecule for the first time

A Danish research group at the Department of Nutrition, Exercise and Sports, University of Copenhagen,has just found evidence that the signal molecule Rac1 is important for how insulin works in the body's muscle cells and that the molecule functions poorly in patients with type 2 diabetes. This is the first time that this molecule is linked with insulin resistance and muscle glucose uptake during muscle work.

The group found that Rac1, a molecular on-off switch, is activated by insulin in muscles in healthy people, but that this activation is significantly diminished in muscles in patients with type 2 diabetes.

By comparing normal mice with genetically modified mice without Rac1, the research group was also able to demonstrate that Rac1 is necessary for insulin to activate glucose uptake in muscles. As this is the very mechanism which is defective in diabetes patients, these findings are an exciting step on the way towards identifying the mechanisms triggering the defects in type 2 diabetes.

The discovery was recently published in the highly respected American journal Diabetes and was found to be of such interest that it merited editorial comment.

- Our findings show that the Rac1 molecule's function in patients with type 2 diabetes is diminished and thus provide us with a new explanation for why diabetics are insulin-resistant, says Professor Erik A. Richter, DMSc, the head of the research group.

In another study, which has also been published in Diabetes, and also with an editorial comment, the group demonstrated that Rac1 is activated during exercise and is important to muscle glucose uptake during muscle work. It has been known for decades that exercise has a beneficial effect on diabetes by stimulating muscle glucose uptake, but not why this is so.

- Our research indicates that Rac1 may be a part of the explanation as to why exercise can have a beneficial effect on type 2 diabetes, says PhD Student Lykke Sylow, a member of the research group.

- The new research findings represent an important step on the way towards understanding the mechanisms underlying muscular defects in diabetes patients and how exercise may improve the condition. This understanding is extremely important to being able to treat and prevent type 2 diabetes, says Associate Professor Thomas Elbenhardt Jensen, a member of the research group.

Type 2 diabetes is linked to obesity and inactivity and is seeing explosive growth all over the world at the moment. More than 330 million people worldwide are suffering from type 2 diabetes, and the figure is expected to grow to more than 500 million in 2030.

Link to the scientific articles:


http://diabetes.diabetesjournals.org/content/62/6/1865.abstract
http://diabetes.diabetesjournals.org/content/62/4/1139.abstract

Contact

Erik A. Richter, professor, DMSc
Department of Nutrition, Exercise and Sports
Faculty of Science
University of Copenhagen

Mobile: +45 28751626