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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
explained.
"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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