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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.



   ........... BIOLOGY_AGING
                                AGE Breakers
     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
   LISA MELTON, who has a Ph.D. in immunology, is a science writer and
   television researcher based in London. She has an unfortunate penchant
   for cake.

WB0DPN - Pueblo, Colorado
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