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Just out Evidence Of How Big Glucose Damages Blood Vessels Could Lead To New Treatments

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New evidence of how the elevated glucose levels that eventuate in diabetes damage blood vessels may lead to romance strategies for blocking the destruction, Medical Institute of Georgia researchers say. They inaugurate a decreased ability of blood vessels to relax resulted from increased activity of a customary mechanism for altering protein arrangement and function, says Dr. Rita C.Tostes, physiologist in the MCG Institute of Medicine.
The researchers suspect increased altering of proteins by a glucose-derived molecule is a player in vascular problems associated with hypertension, stroke and obesity as well.
One aftermath of eminent glucose levels is low levels of the dynamic vasodilator nitric oxide in blood vessels, a shortfall that increases the risk of high blood energy and eventual narrowing of the vessels, researchers reported at the American Sovereign state of Hypertension 24th Annual Scientific Programme in San Francisco during a seam session with the Council for Flying Blood Pressure.
"We cognize diabetes is a dominant risk factor for cardiovascular disease and we esteem this is one of the reasons," Dr. Tostes says.
Diabetes increases the risk of cardiovascular disease such as heart disease and stroke, yet when glucose, or blood sugar, levels are under control. In fact, approximately 75 percent of humans with diabetes die from some cast of heart or blood vessel disease, according to the American Passion Association.
Most of the glucose in the item goes directly into cells where it's modified to constitute the energy source ATP. However about 5 percent of all glucose is converted to another sugar moiety, O-GlcNAc, one of the sugar types that can modify proteins.
Inside the blood vessel walls of healthy mice, MCG researchers found increased animation by O-GlcNAc competes with another mechanism for modifying proteins called phosphorylation. In blood vessels, phorphorylation modifies the enzyme that produces nitric oxide, called nitric oxide synthase, so that it makes also of the blood vessel dilator. But add bounteous O-GlcNAc to the mix and it seems to beat phosphorylation to the punch so there is the inverse result. The longer O-GlcNAc levels were high, the worse the resulting problem, says Victor Lima, a graduate undergraduate at the University of Sao Paulo working with Dr. Tostes.
An animal example of hypertension seemed to confirm the finding that the another O-GlcNAc, the and blood vessels business agreement over these animals had higher O-GlcNAc levels. "Now we are trying to see why this is ongoing and what comes first. Is increased blood coercion leading to changed O-GlcNAc or are augmented levels of O-GlcNAc contributing to the change we peep in the vasculature of hypertensives?" Dr. Tostes says. "If we know how this changes vascular function, we can conceive some of the dysfunction that we see in diabetes."
To produce definite they were targeting the O-GlcNAc sugar and not dealing with other effects of glucose on blood vessels, the researchers blocked the enzyme OGA, an enzyme that normally removes O-GlcNAc from proteins so they can revert to their average state.
Whether the findings continue to clutch true, drugs comparable to those they use in the lab to inhibit OGA or OGT, the enzyme that adds O-GlcNAc to the protein, could one period hand intersect the cogent cardiovascular risk associated with diabetes, Mister Lima says. "I consider it looks authentic promising," Dr. Tostes adds.
Prospect studies will encompass blocking the pathway for adding O-GlcNAc in hypertensive animals to discover the vigour on blood pressure and vascular function.
Source
The Medical College of Georgia
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