Obesity is an American epidemic. More than 40 percent of Americans are obese. This is not an ideal situation since obesity is a harbinger of coronary heart disease, diabetes, hypertension and some types of cancer. Now, Harvard scientists have found a possible solution to break down that extra body fat.

In a study published in the journal Nature Metabolism, diet-induced obese mice models were able to improve insulin sensitivity and glucose tolerance while resolving obesity-induced inflammation when they were subjected to cold temperatures around 40 degrees Fahrenheit.

“Extensive evidence indicates that obesity and metabolic syndrome are linked with chronic inflammation that leads to systemic insulin resistance, so interrupting inflammation in obesity could offer promising therapies for obesity-related disease,” said co-author Yu-Hua Tseng, professor of medicine at Harvard Medical School.

During the study, the mice were fed a standard high-fat western diet which led to obesity development in them. These mice models were compared to control group animals which were maintained at a thermoneutral zone- the temperature at which the body does not need to generate heat to maintain its core temperature.

The researchers from Brigham and the Joslin Diabetes Center found that the mechanism was dependent on brown adipose tissue or “good fat.” When exposed to cold temperatures, these fat tissues released a naturally occurring molecule called Maresin 2.

“We discovered that cold exposure reduced inflammation and improved metabolism in obesity, mediated at least in part by the activation of brown adipose tissue. These findings suggest a previously unrecognized function of brown adipose tissue in promoting the resolution of inflammation in obesity,” Tseng added.

Maresin 2 was found to play a pivotal role in the experiment.

“We found that brown fat produces Maresin 2, which resolves inflammation systemically and in the liver,” said co-author Matthew Spite, Associate Professor of Anesthesia at Harvard Medical School. “These findings suggest a previously unrecognized function of brown adipose tissue in promoting the resolution of inflammation in obesity via the production of this important lipid mediator.”

The results suggest that Maresin 2 could be used in clinical therapy for patients with obesity, metabolic disease, or other diseases linked to chronic inflammation. Unfortunately, the lipid mediator breaks down quickly in the body. Tseng and colleagues wish to find a more stable chemical analog of Maresin 2 for clinical use.

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