The Bittersweet Truth

Taste receptor cells are not confined to the oral cavity. The gut and pancreas are inundated with taste receptor cells. Taste cells in the gut and pancreas do not convey the sensation of taste to the brain. Instead, they are responsible for sensing nutrients and maintaining the balance of hormones essential in metabolic processes. Activation of these receptors by their respective sweet or bitter substances triggers the release of hormones that regulate appetite and satiety and help maintain appropriate glucose levels in the blood stream. This observation has drawn a plausible link between dysfunction of taste receptor cells and the emergence of diseases such as obesity and diabetes.

Sweet taste receptors in the enteroendocrine cells (cells that secrete hormones) of the gut and pancreas are suggested to play an important role in nutrient sensing and sugar absorption, both processes necessary for energy and maintaining a normal metabolism. When sweet taste receptors sense sugars, they elicit the release of gut hormones. One such hormone, glucagon-like peptide 1 (GLP-1), is responsible for facilitating the absorption of glucose into the bloodstream, enhancing insulin secretion in the pancreas and regulating appetite. Disruptions in any of these physiological processes can result in the development of type II diabetes. In a study aiming at quantifying the levels of sweet taste receptors in the upper gut of healthy and diabetic individuals, researchers observed that the levels of sweet taste receptors were diminished in diabetic type II subjects with elevated blood glucose concentrations. This observation was consistent with previous results showing that type II diabetes patients secreted low levels of GLP-1 in response to a meal in comparison to healthy individuals.

Sweet taste receptors in the gut and pancreas also “taste” artificial sweeteners, also known as non-nutritive sweeteners (NNS). Several research groups found that exposure of mouse cells to sucralose, the sweetener in Splenda, caused the release of GLP-1.