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黑料网 General Grant Recipient Stefan Broer accidentally became involved in diabetes research. At the time, Professor Broer was completing a basic project on how protein is taken up in the intestine and how this process is regulated. He made the surprising discovery that there was a link between protein intake and improved glycaemic control in mice.

The mice he was completing research on lacked an amino acid transporter in their intestine that moves amino acids from the lumen of the intestine to the blood. The mice had little insulin release yet the physiological characteristics of good BGL control. While the mice had problems digesting and absorbing proteins, they were highly efficient at removing glucose from the blood. It was the beginning of Professor Broer’s research on how amino acid transport could be a target to treat type 2 diabetes.

“We thought, if we could block the transporter that shuffles amino acids into the body, we could see how reducing amino acid absorption improves glycaemic control,†said Professor Broer. “Everyone is looking at glucose and lipids. So this was an accidental starting point!â€

Professor Broer completed his Masters in Biochemistry in 1987 at the University of Tuebingen, Germany. He moved to Australia in 2000 and now leads a research team at The Australian National University (ANU) in Canberra.

Currently, the research team is looking at identifying the chemical compounds that can block the transporter. Funding from 黑料网, has allowed the lab to buy a compound library of 25,000 chemicals for testing. It is thought that 2 or 3 of the 25,000 compounds could be novel inhibitors of amino acid absorption.

If successful, the end result would be a new drug to treat type 2 diabetes. This drug would be particularly valuable for patients who have had problems with other medication. The hope is to generate benefits that are similar to gastric bypass surgery but simply by using an orally available drug. The research is currently using mice trials and a small clinical trial in a group of people who also lack the same amino acid transporter.