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Diabetes Linked to Blood Vessel Inflammation
Date:12/6/2007

Easing the blood sugar disease may help the heart, researchers say

THURSDAY, Dec. 6 (HealthDay News) -- U.S. researchers say they've identified a new pathway that increases a dangerous inflammation of blood vessels in people with diabetes.

A team at the University of California, Davis, Health System believes that good control of diabetes may reduce this inflammation and possibly reduce the risk of cardiovascular disease.

They found that people with type 1 diabetes have increased expression and signaling of two key receptors within the innate immune system. These receptors (TLR2 and TLR4) are part of a family of pattern-recognition receptors called Toll-like receptors (TLRs).

Increased expression of TLR2 and TLR4 in people with type 1 diabetes contributes to inflammation of blood vessels, the study authors said. Their finding is published in the online issue of the Journal of Clinical Endocrinology & Metabolism.

"It is not unreasonable to speculate that TLR2 and TLR4 promote (cardiovascular disease) by contributing to the pro-inflammatory state in type 1 diabetes," lead author Ishwarlal Jialal, director of the Laboratory for Atherosclerosis and Metabolic Research, and professor of internal medicine at UC Davis, said in a prepared statement.

"Inflammation is central to heart disease, playing a pivotal role in plaque formation and stroke. We may well find that a serendipitous byproduct of controlling diabetes is the simultaneous control of this new pathway, leading to less inflammation and lower risk of heart problems," Jialal said.

The researchers plan further studies to investigate the molecular mechanisms that cause increased TLR2 and TLR4 expression and how these receptors contribute to inflammation in people with diabetes.

More information

The U.S. National Institute of Diabetes and Digestive and Kidney Disease has more about diabetes, heart disease and stroke.



-- Robert Preidt



SOURCE: University of California, Davis, news release, Nov. 27, 2007


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