The Monell Chemical Senses Center has been conducting research on sweet taste for years, dating back to the discovery of the mammalian sweet taste receptor TAS1R2-TAS1R3 in 2001. This receptor, found in taste bud cells, conveys sweetness when activated and is also expressed in intestinal cells. Recent studies have delved into the role of the sweet-taste receptor in regulating glucose metabolism and its potential implications for managing metabolic disorders such as diabetes. Understanding how this receptor influences glucose tolerance and insulin levels could provide insight into how to better handle glucose in the body.
In a study led by Monell Member Paul Breslin, researchers found that stimulating and inhibiting the TAS1R2-TAS1R3 receptor had different effects on glucose metabolism in humans. An agonist like sucralose, a zero-calorie sweetener, or an antagonist like lactisole, a sodium salt that inhibits sweetness, altered glucose tolerance in various ways when mixed with a glucose meal. These findings highlight how taste receptors can play a role in regulating metabolism and nutrient processing throughout the body.
Plasma insulin levels were measured in participants during an oral glucose tolerance test, showing that sucralose increased insulin release to a glucose load, while lactisole tended to slow insulin release. The study suggests that using TAS1R2-TAS1R3 to anticipate glucose appearance in the blood could help the body handle glucose more effectively. This system of taste receptors throughout the body, including in major metabolic regulatory tissues like the pancreas, liver, and fat cells, allows for constant monitoring and regulation of glucose levels in response to food intake.
The relationship between metabolic health and TAS1R2-TAS1R3 receptor activity is likely significant, as the degree of receptor activation can have acute effects on plasma glucose and insulin levels. The team believes that excessive consumption of sugary foods and beverages could overstimulate the sweet taste receptor, contributing to improper glucose regulation and the development of metabolic syndrome. Future studies should investigate the potential therapeutic benefits of manipulating TAS1R2-TAS1R3 activity to improve metabolic control in individuals at risk for metabolic disorders.
By leveraging Monell’s expertise in the chemical senses, the research team hopes to apply their findings to promote healthier eating habits. Understanding how the sweet taste receptor influences glucose metabolism could lead to interventions that improve metabolic health and prevent the development of chronic diseases like heart disease, stroke, and diabetes. Ultimately, small positive metabolic changes could have significant long-term impacts on the health and well-being of individuals worldwide.