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.