The sweet taste receptor could potentially serve as the first line of defense in a sugar monitoring system within the body. It is also present in specific cells in the intestines, where it may aid in the absorption and processing of glucose as part of this system. A recent study discovered that both stimulating and inhibiting the sweet receptor can help regulate glucose metabolism in humans, with potential implications for managing metabolic conditions like diabetes. The Monell Chemical Senses Center has a strong history of research in the area of sweet taste, with scientists from Monell being part of a team in 2001 that first identified and described the mammalian sweet taste receptor.
The rich research portfolio of the Monell Chemical Senses Center on sweet taste goes way back: Monell scientists were one of four teams in 2001 that found and described the mammalian swe rnrnThe sweet taste receptor, TAS1R2-TAS1R3, was discovered two decades ago. In 2021, Monell researchers published two papers in Mammalian Genome, covering the genetics of mice that have a preference for sugar.
The sweet taste receptor is found in taste bud cells and is responsible for detecting sweetness when activated in the mouth. A recent study in PLOS One, led by a different Monell researcher, explored the possibility of the sweet taste receptor being the initial detection point in a metabolic monitoring system for sugar. The receptor is also present in specific intestinal cells, where it may aid in the absorption and assimilation of glucose as part of this system.
Researchers discovered that activating and deactivating TAS1R2-TAS1R3 can help regulate glucose metabolism in humans, which could have implications for managing metabolic disorders like diabetes. Glucose is the main type of sugar in human blood and serves as a crucial energy source for cells.
Lead author and Monell Member Paul Breslin, PhD, who is also a Professor of Nutritional Sciences at Rutgers University, explained, “Our goal was to investigate the impact of TAS1R2-TAS1R3 on glucose metabolism in both directions.”
The study demonstrated that using a TAS1R2-TAS1R3 activator (sucralose, a zero-calorie sweetener) or aThe TAS1R2-TAS1R3 antagonist lactisole, a sodium salt that inhibits sweet taste, when mixed with a glucose meal, had different effects on human glucose tolerance. This study found that the receptor impacts blood glucose and insulin levels differently depending on whether it is stimulated or inhibited. This suggests that taste receptors play a role in regulating metabolism and nutrient handling. Plasma insulin levels were also impacted by the antagonist.The research measured the sweetness perception of sucralose and lactisole in participants undergoing an oral glucose tolerance test (OGTT). The OGTT involves monitoring blood sugar levels before and after consuming a liquid meal with glucose. The study found that the perceived sweetness of sucralose was linked to early increases in plasma glucose and insulin levels. This means that adding sucralose to the OGTT led to a faster release of insulin in response to the glucose load. Conversely, participants’ sensitivity to the inhibition of sweetness by lactisole was associated with decreased plasma glucose levels and a slower release of insulin.
“When glucose activates taste receptors before being absorbed into the body, it sends signals through the mouth and intestine to regulatory organs like the pancreas. We could potentially find ways to utilize TAS1R2-TAS1R3 to help the body manage glucose more effectively by predicting when glucose will enter the bloodstream,” Breslin suggested. When the body detects glucose, it accelerates absorption to supply glucose to tissues that may require it and possibly to also prevent glucose from progressing too far along the intestine, which may not be beneficial for maintaining a healthy gut microbiome.
“This mechanism is simple and sophisticated in its design.Breslin said, “The same taste receptor is found throughout the body, including the mouth, gastrointestinal tract, pancreas, liver, and fat cells, which are all crucial for regulating metabolism 24/7.”
The researchers believe there is a connection between a person’s health and the activity of their TAS1R2-TAS1R3 receptors. They suggest that the level of receptor activation has immediate effects on plasma glucose and insulin levels and their timing, which is important for metabolic health.
The team suggests that the current excessive dietary habits generally have a negative effect on the activity of TAS1R2-TAS1R3 receptors.Consuming high levels of sucrose, high fructose corn syrup, and high-potency sweeteners may overly stimulate TAS1R2-TAS1R3, which can lead to improper regulation of blood glucose. This can result in a diagnosis of metabolic syndrome, a group of risk factors such as elevated plasma glucose and insulin insensitivity (in addition to obesity, hypertension, and elevated plasma fats) that increases the risk of heart disease, stroke, and diabetes. The authors suggest that future research should investigate the impact of TAS1R2-TAS1R3 stimulation and inhibition in individuals at risk for metabolic syndrome to determine potential therapeutic effects.The potential of manipulating TAS1R2-TAS1R3 for improved metabolic control is being explored, rather than making it worse. According to Breslin, studies using Monell’s expertise in the chemical senses have shown that the sweet taste receptor TAS1R2-TAS1R3 can regulate glucose levels differently depending on the sweetness of the consumed food or drink. The team’s goal is to apply this knowledge to promote healthier eating and drinking habits. Breslin also emphasized that even a small positive metabolic change can significantly impact human life and health over the long term and across a large population.
