By John Ericson
Obesity may make sweets less sweet, according to a new study. Researchers from the University of Buffalo have discovered that in severely overweight mice, the tongue’s reaction to sweet stimuli is significantly less pronounced. The findings may help us understand how the current obesity epidemic transforms the way we interact with food.
Published in the journal PLOS ONE, the study sought to quantify an obese individual’s physical reaction to a food category that tends to figure prominently during the development of the disease: sweets. Although previous inquiries have assessed the influence of obesity on nerves and peripheral taste systems, the current study is the first to focus on the tongue’s actual taste cells. “Studies have shown that obesity can lead to alterations in the brain, as well as the nerves that control the peripheral taste system, but no one had ever looked at the cells on the tongue that make contact with food,” lead author Kathryn Medler said in a press release. “What we see is that even at this level – at the first step in the taste pathway – the taste receptor cells themselves are affected by obesity.”
To investigate, the researchers analyzed gustatory perception in a mouse model of obesity. Basically, this means that they looked at the tongues of severely overweight lab mice. Intriguingly, they found that the average tongue’s reactive capacity differed greatly from that of normal mouse tongues. “The obese mice have fewer taste cells that respond to sweet stimuli, and they don’t respond as well,” Medler said.
So far, the researchers have yet to determine whether this deficiency helps sustain obesity. According to Medler, it is possible that an inability to detect sweets may cause obese people to compensate with more food. “If we understand how these taste cells are affected and how we can get these cells back to normal, it could lead to new treatments,” she said. “These cells are out on your tongue and are more accessible than cells in other parts of your body, like your brain.”
Medler and her colleagues’ study is the latest in a growing series of inquiries into biological factors thought to drive the obesity epidemic. In a study published earlier this year, another team of researchers described how a faulty appetite hormone may make it more difficult for obese people to limit their eating. Like the dulled taste cells, the misfiring glucagon hormone messes with the patient’s ability to achieve satiety, or fullness.