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Belly fat can be deadly, and is linked to a host of chronic diseases, including heart disease and type 2 diabetes. But as many of us probably know, it can be hard to lose weight in this area. Now it seems that inflammation of immune cells may be to blame, and we may be able to use drugs to help us burn off our belly flab.
Christina Cammel, of the Yale School of Medicine, and her colleagues have been investigating macrophages – immune cells that normally track down and gobble up pathogens in the body. But as we age, there’s evidence that the macrophages in belly fat become inflamed.
To see what effect this might have, Cammel’s team isolated macrophages from the fat tissue of young and old mice, and sequenced the DNA from these cells. They found that the genomes of the aged macrophages expressed more genes that hinder a group of molecules that spread signals between nerve cells, called catecholamines.
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The genes do this by activating an enzyme that suppresses these neurotransmitters. The boosted activity of this enzyme in aged immune cells in the belly fat of older mice effectively block signals telling the body that there is fat there that is available to burn for energy.
“We found [that] macrophages in belly fat interfere with signals in a way that’s new to us,” says Cammel.
Antidepressant effect
When the action of a receptor that is involved in the inflammation of immune cells was dampened-down, they found that neurotransmitter signals returned to normal and older mice were able to burn belly fat as rapidly as younger mice after a 24-hour fasting period.
A drug was then used to mess with the enzyme, lots of which was found in aged immune cells. Blocking this enzyme had a similar effect, and older mice were able to burn off the fat around their middle again.
The drug used is a common antidepressant called clorgyline, which is given to some people because low levels of catecholamine have been linked to symptoms of depression.
But we don’t know yet if people taking this drug get any positive side effects on their waistlines. It may be tricky to find out, says Cammel, because the drug also causes changes in appetite. How it does this is unclear – there’s evidence of the drug both boosting and decreasing appetite in people.
In any case, the findings are promising. They have shown that it’s possible to manipulate inflammation and fat metabolism in laboratory animals, says Matt Kaeberlein, at the University of Washington, in Seattle. “There’s no biological reason to think this will be more difficult in humans.”
Journal reference: Nature, DOI: 10.1038/nature24022
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