THURSDAY, Dec. 6 (HealthDay News) -- Obesity and type 2 diabetes are clearly intertwined, but researchers say they've found a way to weaken the connection between the two -- at least in mice.
The key, they say, is blocking the body's inflammation response to high-fat foods.
In this study, published online Dec. 6 in the journal Science, the researchers turned off the JNK (pronounced "junk") genetic pathway in mice, and fed the rodents high-fat diets. Even though the mice became obese, they didn't develop insulin resistance, a forerunner to diabetes.
Other similarly stuffed mice with intact JNK pathways, however, became insulin resistant.
Although the results look promising, it's too early to say whether the findings might apply to humans.
"Everybody has these genes, and they're present within all cells of your body all the time," said study author Roger Davis. "What they do is respond to the diet that you're eating. So if you eat a high-fat, cafeteria diet, it leads to the activation of the protein products -- the enzymes -- of these genes."
Davis, a professor at the University of Massachusetts Medical School and investigator at the Howard Hughes Medical Institute in Worcester, Mass., and his colleagues studied hundreds of mice over multiple years to examine the relationship between inflammation and diabetes.
"What we discovered is the JNK genes in the macrophages are critical for the ability of macrophages to cause inflammation, specifically in response to feeding or eating a high-fat diet," Davis said.
Macrophages -- white blood cells -- attack foreign invaders of the body. They fight infection but their inflammatory response can be harmful too. Inflammation has been linked to conditions such as arthritis, heart disease and cancer.
In the study, mice, "by not having the JNK genes in the macrophages, it prevents the inflammation
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