Researchers Identify Internal Fat 'Furnace' in Mice

Join Our Community of Science Lovers!


On supporting science journalism

If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.


Americans spend nearly $33 billion a year on weight-loss products and services to combat ever-increasing waistlines. But as the prevalence of obesity keeps rising, scientists continue to search for a more thorough understanding of the factors that make some people more susceptible to weight gain than others. To that end, findings published in the current issue of the journal Science could help. Researchers have identified the mechanism behind an internal fat "furnace" in mice that helps the animals stave off excess poundage.

The researchers studied a process known as diet-induced thermogenesis (DIT), in which the body attempts to avoid gaining weight by turning excess calories into heat energy. Previous research had implicated the sympathetic nervous system--particularly a group of molecules known as beta adrenergic receptors (betaARs)--as integral to this conversion. Eric S. Bachman of the Beth Israel Deaconess Medical Center and Harvard Medical School and his colleagues thus engineered a strain of mice that lacked the three known beta-ARs. The team then fed one group of these so-called beta-less mice a fat-laden diet while a second group ate a regular diet of rodent chow. Those animals that lacked beta-ARs and ate the high-calorie foods grew massively obese. "Both the beta-less mice and the control mice ate the same amounts, but because the beta-less group could not expend the extra calories, they grew fat," Bachman says. In fact, the beta-less mice gained an average of 26 grams, whereas control mice eating fatty foods gained only seven.

The findings confirm that betaARs serve to ignite the process of DIT, as well as DIT's role in preventing obesity. "In the control mice, it was clear that a process was 'switched on' as soon as they were fed diets high in fat and calories," study co-author Bradford Lowell says. More research is needed to determine what parallels, if any, the process has in humans. But if scientists can successfully manipulate a similar mechanism in people, perhaps one day we will be able to eat our cake and stay thin, too.

It’s Time to Stand Up for Science

If you enjoyed this article, I’d like to ask for your support. Scientific American has served as an advocate for science and industry for 180 years, and right now may be the most critical moment in that two-century history.

I’ve been a Scientific American subscriber since I was 12 years old, and it helped shape the way I look at the world. SciAm always educates and delights me, and inspires a sense of awe for our vast, beautiful universe. I hope it does that for you, too.

If you subscribe to Scientific American, you help ensure that our coverage is centered on meaningful research and discovery; that we have the resources to report on the decisions that threaten labs across the U.S.; and that we support both budding and working scientists at a time when the value of science itself too often goes unrecognized.

In return, you get essential news, captivating podcasts, brilliant infographics, can't-miss newsletters, must-watch videos, challenging games, and the science world's best writing and reporting. You can even gift someone a subscription.

There has never been a more important time for us to stand up and show why science matters. I hope you’ll support us in that mission.

Thank you,

David M. Ewalt, Editor in Chief, Scientific American

Subscribe