Overweight Hispanic Kids Show Early Markers for Diabetes
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WEDNESDAY, Feb. 27 (HealthDay News) -- A small U.S. study found that obese Hispanic children and adolescents with normal blood sugar levels had elevated markers for blood vessel inflammation that may put them at risk for both type 2 diabetes and cardiovascular disease.
Researchers at the Joslin Diabetes Center studied 38 Hispanic youngsters, aged 10 to 18. Of those, 17 were lean and 21 were obese but had normal blood sugar levels, which means they had not yet developed diabetes.
The obese children had significantly higher percentages of body fat than the lean children and were already showing signs of insulin resistance, a pre-diabetes condition.
The study also found that the obese children had higher levels of blood markers for subclinical, or asymptomatic, inflammation of the inner layer of blood vessels.
"They are already exhibiting problems with circulation. There is an inflammatory process going on in the vessels," lead investigator Dr. A. Enrique Caballero, director of Joslin's Latino Diabetes Initiative, said in a prepared statement.
The findings suggest the obese children may be at increased risk of developing cardiovascular disease at a young age, said Caballero, who is also an assistant professor of medicine at Harvard Medical School.
The study is published in the March issue ofDiabetes Care.
Genetic and lifestyle factors put Hispanic children at high risk for developing type 2 diabetes, but they had not previously been studied, Caballero said.
"We have found that overweight Hispanic children and adolescents have elevated markers of endothelial dysfunction and vascular inflammation closely related to excess body fat and increased insulin resistance," the study authors concluded. "This ... may increase their risk of developing type 2 diabetes and cardiovascular disease, further emphasizing the need for obesity prevention strategies."
More information
For more on preventing diabetes, visit the American Diabetes Association.
SOURCE: Joslin Diabetes Center, news release, Feb. 27, 2008



