Sucralose regulates postprandial blood glucose in mice through intestinal sweet taste receptors Tas1r2/Tas1r3.

Long-term consumption of sucralose may increase body weight and the risk of elevated PBG, resulting in over expression of sweetness receptors and glucose transporters. The mechanism of these effects might be the result of non-nutritive sweeteners binding to sweetness receptors Tas1r2/Tas1r3 in gut endocrine cells and up-regulating Slc5a1 and Slc2a2. But we can't rule out that the rise in PBG is the result of a combination of sweet receptors and gut microbes. Therefore, the effect of gut microbes on PBG needs to be further studied. This article is protected by copyright. All rights reserved.