Thursday, November 06, 2008
"The red wine weight loss wonder drug that lets you eat junk food"
Anything that "mimics" resveratrol or red wine is ipso facto suspect as a therapeutic agent. The red-wine/resveratrol theory is a great fad but resveratrol does NOT do many of the things claimed for it when properly tested -- such as prolong life
For dedicated couch potatoes, it sounds almost too good to be true. A drug inspired by red wine could allow them to eat as much junk food as they like without putting on a pound. It could also provide the benefits of exercise without moving a muscle. And if that were not enough, the pill - which mimics the action of resveratrol, the 'wonder ingredient' in red wine - may also prevent diabetes.
The man-made drug, which is known only as SRT1720, fools the body into thinking food is scarce and it has to burn off fat to survive. The brainchild of scientists at US firm Sirtris, the drug exploits the healthy qualities of resveratrol, a chemical found in grape skins. Previous studies have endowed resveratrol with the ability to ward off a host of ills, from old age to heart disease, cancer, obesity and Alzheimer's disease.
Sirtris has already developed a concentrated form of resveratrol in a pill. However, the new drug could be even more powerful and have fewer side-effects. David Sinclair, co-founder of Sirtris, which is now owned by Glaxo-SmithKline, said recently: 'The excitement here is that we are not talking about red wine any more. We are talking about real drugs.'
In experiments, mice given SRT1720 didn't gain an ounce, despite being fed fatty foods. Blood tests suggested they were also protected against diabetes. The treated animals also had more stamina and were able to run twice as far. However, they had to be forced to exercise. Left to their own devices, they would move around less than normal, the journal Cell Metabolism reports. [A very discouraging side-effect, one would think]
The drug is made up of chemicals that affect the body in a similar way to resveratrol. Both resveratrol and the new drug trigger a protein called SIRT1 that plays a key role in regulating the body's supply of energy. The result is that the body burns off its fat stores, even when food is plentiful.
Researcher Professor Johan Auwerx, of the Ecole Polytechnique Federale de Lausanne in Switzerland, said: 'These results show that new synthetic SIRT1 activators can reproduce the positive metabolic effects that were previously demonstrated using resveratrol. 'But unlike resveratrol, these new chemical entities target only the SIRT1 pathway, making them more selective and potent for achieving these metabolic benefits.' He added that the drug, which is around seven years from the market, is likely to be used to treat obesity and diabetes.
Prof Ian Broom, an obesity expert from Robert Gordon University in Aberdeen, said any drug that burnt off fat while protecting against diabetes would be welcomed. But he cautioned that much more research - including studies into side-effects - would be needed before SRT1720 became accepted as a treatment for obesity.
Source
PhD student unlocks diabetes insulin mystery
AUSTRALIAN scientists have uncovered a key clue in the mystery of how insulin works, bringing them closer to a cure for diabetes. A Sydney PhD student Freddy Yip has solved a problem plaguing researchers worldwide for more than half a century - how insulin prompts fat and muscle cells to absorb glucose. This process is defective in the growing number of people with type 2 diabetes so understanding it opens the way for new therapies to correct it.
"While we're certainly not saying we've found a way to cure diabetes, we are saying we've found a pretty significant clue," said David James, head of the diabetes program at the Garvan Institute for Medical Research. "Since the 1920s, when Banting and Best discovered insulin, scientists have been battling to discover how it actually works," Professor James said. "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."
The findings, published in the journal Cell Metabolism, focus on two intersecting problematic processes affecting diabetics, insufficient production of insulin in the pancreas after a meal and so-called insulin resistance, and the faulty uptake and storage of glucose in fat and muscle cells. "In the cell we have series of motor proteins that have the ability to move other molecules from one place to another along intracellular railroad tracks," Mr Yip 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." The motor protein helps move glucose transporter proteins from inside the cell to the surface membrane so that they can pump glucose into the cell.
The findings offer up a new target for diabetes treatment. "We think there may be blockages in the signal between insulin and myo1c in people who develop insulin resistance," he said. "If we're correct, it should be possible to target that pathway for development of new therapies." Statistics show about 700,000 Australians suffered diabetes in 2005, a figure which has doubled since 1981.
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