The sweet tooth that compels some people to snack on candy and sugary foods is really more of a sweet tongue. A new study of mice by Japanese researchers suggests that the same hormone that the brain uses to regulate appetite can also lessen a tongue’s penchant for sweet substances.
By doing so, the hormone, known as leptin, provides the body with another way to control its intake of calories, speculate taste physiologist Yuzo Ninomiya at the Kyushu University in Fukuoka, Japan, and his colleagues.
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“Taste is more than just a passive system telling us if something is sweet, sour, salty, or bitter. It plays a more direct role in the control of food intake than was previously thought,” comments Timothy A. Gilbertson of Utah State University in Logan, who studies how the tongue responds to fatty substances.
Ninomiya and his colleagues discovered the leptin-taste connection when they began studying a mouse strain having a mutation in the gene for leptin’s receptor, the cell-surface protein that the hormone stimulates. Secreted by fat cells, leptin circulates in the blood. Once it reaches the brain, the hormone normally serves as a gauge for how much fat the body has stored and helps regulate hunger (SN: 07/29/95, p. 68).
Because they can’t sense leptin, the mutant rodents eat excessively, become obese, and develop diabetes. Moreover, the pancreatic cells of the receptor-lacking mice are hypersensitive to the sugar glucose. This prompted Ninomiya to wonder whether the taste cells in these mice are hypersensitive to sugars as well.
The mutant mice did indeed have a greater fondness for sweet substances than normal, lean mice did, the researchers found.
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Suspecting that leptin suppresses sensitivity to sweetness, the team then tested taste buds from the mutant mice. The sensory cells of these buds responded to sugars more strongly than cells from normal mice did.
The Japanese team’s new work, to be reported in the Sept. 26 Proceedings of the National Academy of Sciences, firms up the leptin-taste connection. In one experiment, Ninomiya’s group injected leptin into normal mice. Within 10 minutes, a sensory nerve in the tongue decreased its responsiveness to sucrose and saccharin. The nerve’s reactions to salty, bitter, or sour substances didn’t change.
The investigators also demonstrated that a subset of taste cells on a mouse tongue normally synthesizes a receptor for leptin. They further found that the hormone activates cell-membrane channels that permit potassium ions to rush inward, which makes it more difficult for a taste cell to respond to any stimuli.
From these pieces of evidence, Ninomiya and his colleagues conclude that the tongue is a target for leptin’s actions and that the hormone works to dull the tongue’s sweet tooth. Taste researcher Stephen D. Roper of the University of Miami School of Medicine praises the new leptin study for combining several research techniques to tell a persuasive story. “The paper is very solid,” he says.
Findings such as this one will bring more attention to the regulation of taste, predicts Gilbertson. “This system is incredibly dynamic. The more we look at it, the more complicated and interesting it becomes. Lots of hormones affect the taste system,” he says.