MELBOURNE, May: Australian researchers have discovered a link between protein intake and improved control of blood glucose in mice, opening the way for potential new treatments for diabetes in human beings.
Lead researcher Stefan Broer of Australian National University (ANU) said the findings show mice, with a reduced capacity to digest and absorb protein, are highly efficient at removing glucose from blood after a meal.
“This is precisely what individuals with diabetes fail to do. This research has significant potential for the design of new drugs to treat type 2 diabetes,” said Professor Broer, from the ANU Research School of Biology.
Around one million Australians suffer from type 2 diabetes and around two million more are at risk of developing the chronic condition, which can severely impact on lifestyle and lead to high blood pressure and weight gain.
Broer said the mice lacked a so-called transporter in the intestine that moves amino acids, the breakdown products of protein digestion, from the lumen of the intestine into the blood.
This reduces the intake of protein and indirectly improves their efficiency at removing glucose from the blood.
The mice also have reduced levels of cholesterol and fat in the blood, which are typically elevated in obese people and can lead to the onset of diabetes.
“What makes these results so exciting is the accessibility of this target in humans.
As a result it is reasonably straightforward to develop a pharmaceutical drug that blocks this transporter.
“If we can replicate in humans what we see in these mice we might be able to develop a new drug to treat type 2 diabetes.
“We are now running a small clinical trial to test this in humans who also miss this transporter due to a rare benign genetic defect,” he said.
The research has been supported by the global healthcare company Sanofi, which produces a variety of treatment solutions for people living with diabetes.
“Without the support from Sanofi we would have not been able to do this important research in Australia,” Broer said. (AGENCIES)
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