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[IP] New drug to help diabetics..??
I got this news story, and thought some on the IP list would find it
interesting. Towards the end of the article, it speaks of a new drug
being tested, that shows promise in undoing the cause of some DM
complications... This either has been printed in Scientific American,
or is soon to be printed.
Rupturing the body's sugar-protein bonds might turn back the clock
LONDON--For all the promise of anti-aging creams and therapies,
nothing has ever restored the vigor of youth or even delayed the
inevitable process of growing old. Researchers now claim to have
developed a compound that might rejuvenate hearts and muscles--by
breaking the stiff sugar-protein bonds that accumulate as we get
Anthony Cerami of the Kenneth S. Warren Laboratories in Tarrytown,
N.Y., suspected some 30 years ago that sugar affects how the body
ages, based on observations of diabetics, who age rapidly. Sugars are
an essential source of energy, but once in circulation they can act as
molecular glue, attaching themselves to the amino groups in tissue
proteins and cross-linking them into hard yellow-brown compounds known
as advanced glycation end products, or AGEs.
Indeed, after years of bread, noodles and cakes, human tissues
inevitably become rigid and yellow with pigmented AGE deposits. For
the most part, piling on dark pigments in the teeth, bones and skin is
harmless. But where glucose forms tight bonds with the long-lived
protein collagen, the result is a constellation of changes, including
thickened arteries, stiff joints, feeble muscles and failing
organs--the hallmarks of a frail old age. (Diabetics age prematurely
because sugar-driven damage acquires breakneck speed, raising their
levels of AGE-infused collagen to those of elderly people.) "The
evidence that sugar cross-linking increases as we age is persuasive,"
comments Jerry W. Shay of the University of Texas Southwestern Medical
Center at Dallas. "There are diseases associated with increased
glycation, which are directly related to increased age." Sugar's
connection with AGE formation may be one reason caloric restriction
might delay aging.
Cerami's quest has been to find an "inhibitor"--a compound that by
tying up reactive glucose might keep it away from susceptible
proteins. To his surprise, the food industry had the answer. Since
1912 chemists have known that in the heat of an oven sugars and amino
acids form tight chemical bonds--a reaction that turns roasted turkey,
toast and coffee to a tasty golden brown. This Maillard chemistry, as
it is known in food circles, is the same sugar-protein bonding that
stiffens our tissues. Crucially, food chemists also discovered that
adding sulfites prevents browning and hardening and keeps food and
beverages looking fresh.
Exploiting this culinary knowledge, Cerami's team showed in the
mid-1980s that aminoguanidine could keep the tissues of diabetic rats
and other old animals as elastic as those of young control subjects.
It boosted their cardiovascular function and improved other
age-related disorders. Further studies showed that aminoguanidine
lowered diabetics' urine albumin--an indicator of kidney
malfunction--and delayed AGE-related damage to the retina.
Perhaps more exciting is Cerami's recent discovery of a molecular
"breaker"--a drug that may actually reverse the aging process by
cracking sugar-protein links once they form. "Instead of looking for
prevention, we can now administer a compound to reduce the stiffness
we see in diabetes and aging," Cerami reported at a recent Novartis
Foundation symposium in London. The breaker,
dimethyl-3-phenacylthiazolium chloride, or ALT-711, can tear tough
AGE bonds apart. Diabetic animals, old dogs and elderly rhesus monkeys
given the compound daily for three weeks yielded spectacular results.
"The heart and major arteries, which were quite stiff, became more
pliable and elastic. So the heart could pump more blood--similar to
what you'd see in a young animal," Cerami stated.
Cerami envisages multiple uses for breakers in pathologies wherein
tissues lose flexibility. In glaucoma, for example, increasing the
elasticity of the draining canal would prevent the buildup of pressure
in the eye. ALT-711 could also renew declining lung elasticity and
soften an enlarged and hardened prostate. But it will be at least 10
years until such drugs, currently undergoing clinical trials, are
approved for humans.
Will breakers stop aging in its tracks? After all, the field of
antiaging drugs is littered with compounds that failed to live up to
their hype or were hardly more than snake oil [see Scientific American
Presents: The Quest to Beat Aging; Summer 2000]. A single
fountain-of-youth elixir is highly unlikely, says Tamara Harris of the
National Institute on Aging, because other activities, such as
free-radical oxidation and possibly telomere shortening, also
contribute to the body's slow decline. Moreover, AGE-related research
tends to be slow: Harris points out that there is no easy,
well-validated way to measure AGE in the body, a shortcoming that
complicates trials. To Harris, however, AGE breakers remain an
appealing option. "This is a nice approach because it is multifocal,
aimed at a basic process that occurs in multiple systems. But," she
warns, "there won't be one silver bullet."
LISA MELTON, who has a Ph.D. in immunology, is a science writer and
television researcher based in London. She has an unfortunate penchant
WB0DPN - Pueblo, Colorado
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