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Completely novel action of insulin unveiled
Published: Wednesday, November 5, 2008 - 09:31 in Health & Medicine
Learn more about: action of insulin garvan institute of medical research 
glucose transporter glucose uptake prestigious international journal production 
of insulin

A PhD student at Sydney's Garvan Institute of Medical Research has uncovered an 
important piece in the puzzle of how insulin works, a problem that has plagued 
researchers for more than 50 years. This finding brings us one step closer to 
explaining exactly how insulin prompts fat and muscle cells to absorb glucose. 
The novel finding by Freddy Yip was published online today in the prestigious 
international journal, Cell Metabolism.

"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."

There are two processes involved in Type 2 diabetes: insufficient production of 
insulin in the pancreas after a meal and faulty uptake and storage of glucose 
in fat and muscle cells, or 'insulin resistance'.

Freddy's finding focuses on the intersection between these two processes. "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 

"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."

Insulin controls glucose uptake into our fat cells by moving glucose 
transporter proteins from inside the cell to the surface membrane so that they 
can pump glucose into the cell. Myo1c aids in this process by helping the 
transporters slide into the surface membrane.

In healthy people, around 80% of the glucose transporters migrate to the cell 
membrane after a meal, allowing plenty of glucose into the cell. In people with 
Type 2 diabetes, however, that figure drops to around 10%.

Freddy Yip believes his study 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."

Professor James sees the finding as a welcome milestone on a very long road of 
discovery. "While we're certainly not saying we've found a way to cure 
diabetes, we are saying we've found a pretty significant clue."

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