Anti-inflammatory drugs can reduce the risk of metabolic disease by inhibiting the sweet taste receptor

Anti-inflammatory drugs can reduce the risk of metabolic disease by inhibiting the sweet taste receptor

Previous studies have shown that the human sweet taste receptor mediates sweet perception in the mouth and may help regulate glucose metabolism throughout the body. At the same time, the anti-inflammatory drugs ibuprofen and naproxen are structurally similar to sweet taste receptor inhibitors and have been associated with metabolic benefits. Researchers from the Monell Chemical Sens Center and Rutgers University have published a study in theBritish Journal of PharmacologyThis suggests that these drugs could be another way to reduce the risk of metabolic diseases by inhibiting the sweet taste receptor throughout the body.

We found that ibuprofen and naproxen inhibit activation of the sweet taste receptor in humans as well as in human cells. We found that when ibuprofen and naproxen inhibit sweet taste by inhibiting the Tas1r2-Tas1R3 taste receptor response to sugar, this may affect glucose metabolism. “

Paul as Breslin, PhD, senior author and Monell member

In the team's cellular studies, ibuprofen reduced sucrose and sucralose molecular signaling in human kidney cells to express the sweet taste receptor. To reflect internal human oral physiology, low concentrations of ibuprofen, approximately the human plasma level after a typical home dose, inhibited the sweet taste and oral detection of glucose at concentrations approximately the blood glucose level as measured.

Connecting the points

Long-term ibuprofen use has been associated with preserved metabolic function and a reduced risk of metabolic diseases such as Alzheimer's disease, diabetes and colorectal cancer. In addition to their anti-inflammatory properties, the team found that ibuprofen and naproxen also inhibit an important blood sugar receptor. For example, in the team's human experiments, when a participant rinses their mouth with ibuprofen, the perception of sweetness from various sugars and sweeteners is reduced.

Evidence from other studies has also shown that ibuprofen reduction and chronic disease risk reduction are intertwined. The most obvious situation, Breslin notes, is type 2 diabetes—if you have elevated blood sugar and take a lot of ibuprofen, your blood sugar increases. The second is a reduced risk of diseases that involve glucose metabolism in certain tissues, such as Alzheimer's and some cancers.

“Our study connects the two functions of Tas1R receptors as the gatekeepers of sugar absorption and as a downstream modulator of glucose metabolism,” said Breslin, also a professor of nutritional sciences at Rutgers University. "In this work, we show that ibuprofen modulates more than inflammation. It is also a Tas1r2-Tas1R3 inhibitor - a receptor expressed in most metabolic regulatory tissues and organs." There is a lot of evidence from previous studies that metabolism can change when you inhibit Tas1r2-Tas1R3 receptors.

“Our work connects the dots,” Breslin said. "What we're trying to say is that when we think about these inflammatory and metabolic diseases - like Alzheimer's and diabetes - if we manipulate the taste receptors expressed in the body, that may have some significance in lowering glucose to reduce the risk of disease."

Other co-authors include Lauren Caronia and Peihua Jiang, both of Monell; and Emily C. Hanselman, Caroline P. Harmon, Daiyong Deng, and Sarah M. Sywanycz, all from the Department of Nutritional Sciences, Rutgers University.

This work was funded by the National Institutes of Health National Institute of Deafness and Other Communication Disorders grants R01 014286 and R21 020365 and New Jersey Hatch project NJ14120.

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