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.
Bitter taste receptors in the stomach are known to confer protection against ingested toxic substances by provoking repulsion towards bitter food. Scientists have recently found that activation of bitter taste receptors in the gut stimulates the production of hormones involved in appetite stimulation. A study in which mice were administered bitter tastants showed that bitter taste receptors induced the release of ghrelin, an appetite-stimulating hormone, resulting in short-term food intake. This was immediately followed by a prolonged decrease in food ingestion, correlating with an observed delay in emptying of the stomach leading to a sensation of satiety. The relationship between the ingestion of bitter compounds and a feeling of fullness suggests new potential directions in the treatment of obesity.
Last week I attended a seminar to update the progress Harvard has made in looking at these gut and organ “taste” receptors. They are in line for a possible Nobel Peace Prize for their research.
Following President Eisenhower’s second heart attack in 1958, government took an active role in altering the American diet. The AMA and others decided that he ate too much red meat and not enough carbohydrates. The food pyramid evolved and the cereal industry boomed. As cereal became popular, the cereal companies began removing the bitter compounds from the grains to make cereal taste better. Wheaties and Cheerios were the most popular brands. The added sugar would come latter, but the damage had already been done and the rest of the food industry followed suit.
The Bottom Line:
The increased consumption of refined carbohydrates set the stage for the epidemic of diabetes and heart disease in America. However, it wasn’t just the food substitution but rather the refining of the grains, removing bitter compounds that help regulate glucose metabolism and satiety that accelerated this process.
Source: May 30, 2013 Harvard University