The Monell Chemical Senses Center’s rich portfolio of research on sweet taste goes back a long way: Monell scientists were one of four teams that in 2001 found and described the mammalian sweet taste receptor, TAS1R2-TAS1R3. Twenty years later, in 2021, a pair of papers published in Mammalian Genome by Monell researchers covered the genetics of sugar-loving mice.
The sweet taste receptor, expressed in the cells of the taste buds, transmits sweetness from the mouth when activated. Earlier this month, a study in Plus one, led by another Monell researcher, delved into how the sweet taste receptor could be the first stop in a metabolic sugar surveillance system. The receptor is also expressed in certain intestinal cells, where it can facilitate the absorption and assimilation of glucose, as part of this system.
The team found that stimulation and inhibition of TAS1R2-TAS1R3 shows that it helps regulate glucose metabolism in humans and may have implications for the management of metabolic disorders such as diabetes. Glucose is the main type of sugar found in human blood, making it a key source of energy for cells.
“Our goal was to determine whether TAS1R2-TAS1R3 influences glucose metabolism in two directions,” said Paul Breslin, PhD, Monell Fellow, professor of Nutritional Sciences at Rutgers University and senior author of the paper.
They showed that a TAS1R2-TAS1R3 agonist (sucralose, a zero-calorie sweetener) or a TAS1R2-TAS1R3 antagonist (lactisol, a sodium salt that inhibits sweet taste) mixed with a glucose meal acutely altered human glucose tolerance of different degrees. ways. Here, an agonist binds to a receptor and stimulates a cell and an antagonist binds to a receptor and prevents stimulation.
“The novelty of our findings is that the receptor we studied in this experiment affects blood glucose and insulin during a glucose meal differently, depending on whether it is stimulated or inhibited,” Breslin said. This work provides additional evidence that taste receptors help regulate metabolism and nutrient management.
Plasma insulin levels were measured in study participants who underwent an oral glucose tolerance test (OGTT), which tracks blood sugar levels before and after a person drinks a liquid meal. containing glucose. Participants’ ratings of the perceived sweetness of sucralose were correlated with early increases in plasma glucose as well as increases in plasma insulin levels when sucralose was added to the OGTT. Added sucralose tended to accelerate insulin release upon glucose loading. On the other hand, participants’ sensitivity to lactisol-driven sweetness inhibition was correlated with a decrease in plasma glucose levels. Lactisol also tended to slow insulin release.
“When glucose stimulates taste receptors before being absorbed by the body, signals are sent through the mouth and intestine to regulatory organs such as the pancreas. Perhaps we could devise ways to use TAS1R2-TAS1R3 to help the body better manage glucose by anticipating when glucose will appear in the blood,” Breslin said. When the body senses glucose, it speeds up absorption to get it to tissues that may need it and possibly also to prevent glucose from moving too much throughout the gut, which may not be good for maintaining a healthy gut microbiome.
“This system is elegant in its simplicity,” Breslin said. The same taste receptor is found throughout the body: the mouth, gastrointestinal tract, pancreas, liver and fat cells, the latter three being important metabolic regulatory tissues, all part of the body’s 24-hour metabolic surveillance. day, 7 days a week.
Is there any relationship between a person’s health status and the activity of their TAS1R2-TAS1R3 receptors? The study authors say that is likely, suggesting that the degree of receptor activation exerts acute influences on plasma glucose and insulin levels and their timing, which is important for metabolic health.
The team maintains that, in general, current dietary habits of excessive consumption of foods and beverages high in sucrose, high fructose corn syrup, and high-potency sweeteners could hyperstimulate TAS1R2-TAS1R3, contributing to the inappropriate regulation of blood glucose. This could lead to a diagnosis of metabolic syndrome, a set of risk factors including elevated plasma glucose levels and insulin insensitivity (along with obesity, hypertension, and elevated plasma fat levels) that increase the risk of heart disease. , strokes and diabetes. The authors say future studies should examine the effects of TAS1R2-TAS1R3 stimulation and inhibition in people at risk for metabolic syndrome to determine the therapeutic potential of manipulating TAS1R2-TAS1R3 for better rather than worse metabolic control.
“Studies like these, using Monell’s technical ability and deep experience in chemical senses, show that the sweet taste receptor TAS1R2-TAS1R3 helps regulate glucose differently, depending on the sweetness of the food or drink,” he said. Breslin. The team’s hope is to apply what they learned to make what we eat and drink healthier.
“A small positive metabolic change can add much more to human life and health when compounded over decades and millions of people,” Breslin said.