Dr. Joel Zonszein, director of the Clinical Diabetes Center at Montefiore Medical Center in New York City, who was not associated with the study, said science in this area has gone beyond realizing that having more body fat -- particularly more "central" or waistline body fat -- is a risk factor for diabetes.
"We have the so-called healthy obese who have less fatty tissue, they have less inflammation, they have less macrophages," Zonszein said. "And we have some people who don't look very obese but their [fat] tissue is loaded with macrophages, particularly bad macrophages."
The new mouse study, Zonszein said, "is one unique pathway that they identified in a very nice way -- because we always have associated obesity with insulin resistance, but in their model [the mice] develop obesity but their insulin's healthy."
Zonszein added, however, that what goes on in the human body is much more complex. "Nonetheless, this is science -- something that we need to learn from. But from this to drug-development implications in humans, there is a big, big stretch," he said.
Study author Davis acknowledged the gap between animal research findings and clinical benefits, but said it might be bridged.
"One possible scenario -- and obviously our work is on mice, so there's a big leap of faith here to establish [this] in humans -- but the work we've done would suggest that drugs that are targeted to JNK kinase genes would be useful for the treatment of diabetes," he said. "But this is definitely a big step beyond the point of our own work."
One take-away message, Davis said, is that eating unhealthy foods immediately affects your body.
"It's useful for people to recognize that the foods they eat have these very direct biochemical effects," he said. "Sometimes people thi
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