| Biomarkers may predict diabetes in women
NEW YORK (Reuters Health) - Elevated levels of biomarkers that
reflect abnormal functioning of cells that line blood vessels and
the heart (endothelial dysfunction) may help doctors identify women
who are at increased risk of developing type 2 diabetes, according
to a new study.
These findings provide new evidence for the hypothesis that endothelial
dysfunction precedes cardiovascular diseases and type 2 diabetes,
Dr. James B. Meigs told Reuters Health.
Meigs of the Massachusetts General Hospital in Boston and colleagues
point out that endothelial dysfunction is seen in diabetics, but
may also precede development of the condition. Identification of
endothelial dysfunction as a type 2 diabetes precursor, they note,
"might expand options for diabetes prevention and treatment."
The researchers evaluated a subgroup of 737 women, who were enrolled
in a larger ongoing study. The subjects were initially free of diabetes,
cardiovascular disease and cancer, but eventually developed diabetes.
These women were compared with 785 control subjects.
At the beginning of the study, levels of biomarkers of endothelial
dysfunction--namely E-selectin, adhesion molecule 1 and vascular
adhesion molecule 1--were significantly higher in cases than controls.
After adjusting for factors such as body mass index and smoking,
those with the highest levels of E-selectin had a risk of diabetes
5.43 times that of those with the lowest levels. Higher levels of
the other two biomarkers also correlated with increased diabetes
risk.
Endothelial dysfunction appears to predict the development of type
2 diabetes in women independent of other known risk factors, the
researchers report in the Journal of the American Medical Association.
"If this hypothesis is supported by additional studies,"
Meigs added, "endothelial dysfunction may be the fundamental
abnormality underlying the insulin resistance syndrome. Thus, therapies
which improve endothelial dysfunction may prove to play an important
role in the treatment of insulin resistance and type 2 diabetes."
SOURCE: Journal of the American Medical Association, April 28,
2004.
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