Protein behind insulins effectiveness in controlling glucose uptake uncovered

November 6th, 2008 - 1:30 pm ICT by ANI  

Washington, November 6 (ANI): A PhD student at Sydney’’s Garvan Institute of Medical Research has made a significant advance towards understanding exactly how insulin prompts fat and muscle cells to absorb glucose, a problem that has puzzled researchers for over 50 years.
“Since the 1920s, when Banting and Best discovered insulin, scientists have been battling to discover how it actually works,” said Professor David James, head of Garvan’’s Diabetes Program.
“Then along comes Freddy Yip, doing his PhD, who unveils a completely novel action of insulin, one which we believe plays a fundamental role in glucose uptake, a process that is defective in Type 2 diabetes,” he added.
Type 2 diabetes involves two processesinsufficient production of insulin in the pancreas after a meal, and faulty uptake and storage of glucose in fat and muscle cells, or ”insulin resistance”.
It is on the intersection between the two processes that Freddys finding focuses on.
“In the cell we have series of motor proteins that have the ability to move other molecules from one place to another along intracellular rail road tracks,” he said.
“I have discovered that insulin activates a specific kind of motor protein known as Myo1c, which in turn performs a critical role in glucose uptake,” he added.
Insulin controls glucose uptake into fat cells by moving glucose transporter proteins from inside the cell to the surface membrane, in order that they can pump glucose into the cell. Myo1c aids in the process by helping the transporters slide into the surface membrane.
Among people with good health, around 80 per cent of the glucose transporters migrate to the cell membrane after a meal, allowing plenty of glucose into the cell. However, in Type 2 diabetics, the figure drops to around 10 per cent.
Freddy believes that his work will create a strong foundation for future diabetes research.
“We knew before that Myo1c was somehow involved in the regulation of glucose transport. My research indicates that Myo1c is a major target of insulin action and helps to accelerate the delivery of transporters to the membrane,” he said.
“We think there may be blockages in the signal between insulin and myo1c in people who develop insulin resistance. If we”re correct, it should be possible to target that pathway for development of new therapies,” he added.
Professor James hailed Freddys work by saying: “While we”re certainly not saying we”ve found a way to cure diabetes, we are saying we”ve found a pretty significant clue.”
The study has been reported in the online edition of the journal Cell Metabolism. (ANI)

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