SAN FRANCISCO (Reuters Health) - Evidence is accumulating that mild, chronic inflammation is somehow associated with the development of type 2 diabetes, the most common form of the disease, researchers reported here Saturday at the American Diabetes Association's annual meeting.

"We have demonstrated that markers of inflammation proceed and predict development of diabetes," said Dr. Bruce Duncan, an associate professor in the school of medicine at the Federal University of Rio Grande do Sul in Brazil.

Type 2 diabetes is associated with obesity and typically develops in older adults. However, with the boom in obesity rates, this type of diabetes is increasingly being diagnosed in young adults and children.

Previous research has suggested that inflammation may play a role in the susceptibility to diabetes, just as doctors have come to realize that inflammatory responses play a role in heart disease, which shares many risk factors with diabetes. However, the role inflammation may play in diabetes is still unclear.

Type 2 diabetes results from the body's inability to correctly use insulin, which leads to excessively high blood sugar levels that can increase the risk of blindness, kidney disease and amputations.

In this research, Duncan and colleagues looked at four markers in the blood that are signs of inflammation. The researchers selected 651 people who developed diabetes and 643 who did not from a larger study of 10,000 individuals followed for 9 years.

They then compared the two groups, looking at four inflammatory markers: C-reactive protein (CRP), orosomucoid, sialic acid and interleukin-6 (IL-6). The researchers took into account factors that may have influenced the development of diabetes, such as age, gender and ethnicity.

Duncan reported that those with the highest level of sialic acid had a 70% higher risk of developing diabetes than those with the lowest level. Duncan also found evidence that all four markers were associated with a twofold to threefold risk of developing diabetes; however, that finding was diminished when adjusting for factors such as body mass index and glucose levels.

"Although studies have been inconsistent, the weight of the evidence is (that) there does exist an association," he noted. "The question is less 'Does it exist?' and more 'Why it exists."'

One theory, according to Dr. Paresh Dandona, head of the division of endocrinology, diabetes and metabolism at the State University of New York at Buffalo, is that food intake can cause an inflammatory response that can be perpetually present among the obese.

The body's anti-inflammatory responses may somehow block the normal functioning of insulin, leading to the development of diabetes, he said. This inflammatory response may help explain why obesity can lead to diabetes and suggest ways to prevent this from happening.

For example, in related research, Dandona presented findings that suggest that certain medications, such the blood-sugar lowering drug rosiglitazone, can reduce certain inflammatory markers by 20% to 40% after 6 weeks of use and may reduce the risk of developing diabetes.

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