How nonnutritive sweeteners can be beneficial for those who don’t normally consume them….
Artificial sweeteners, also known as nonnutritive sweeteners, are food additives that mimic the effect of sugar in taste but with fewer, if any, calories. Because of this, artificial sweeteners have been widely used by consumers to reduce caloric intake as well as glycemic load. Currently there are seven FDA approved nonnutritive sweeteners. Sucralose, a noncaloric nonnutritive sweetener, is about 320-1000 times sweeter than table sugar. Splenda is a brand name example of a sucralose-based sweetener.
Data from previous studies on nonnutritive sweeteners have suggested that although non-caloric, they are not physiologically inert. One such study has shown that places like the gastrointestinal tract and the pancreas can detect sugars through taste receptors that are similar to those found in the taste cells of the mouth. Furthermore, other studies have shown that the activation of sweet taste receptors in the gut by nonnutritive sweeteners can trigger the secretion of glucagon-like peptide 1 (GLP-1) and insulin. Additionally, data from studies conducted in animals have shown that nonnutritive sweeteners can interact with sweet taste receptors in the GI tract and pancreas which can increase intestinal glucose absorption. Although many studies conducted on humans show that nonnutritive sweeteners do not affect plasma glucose, insulin secretion, or GLP-1 secretion, these subjects are usually chronic consumers of nonnutritive sweeteners. This prompted a study on non-chronic users of nonnutritive sweeteners.
This study shows the effects of nonnutritive sweeteners in subjects (specifically obese) that are not regular users of artificial sweeteners. A total of 17 obese subjects who were not regular consumers of nonnutritive sweeteners participated in a crossover study and were studied on two separate occasions approximately 7 days apart. In a randomized order, subjects drank 60 ml of a liquid containing 48 mg sucralose or an equivalent amount of distilled water 10 minutes before a 75 gram glucose ingestion. This particular amount of sucralose was chosen because it is the effective concentration needed to stimulate GLP-1 secretion in human intestinal cells, and it also approximates the amount of sucralose in a 12-ounce can of diet soda. Blood samples were them obtained to assess plasma glucose, insulin, C-peptide, glucagon, GIP, and GLP-1 concentrations at various time intervals before and after the ingestion of glucose. The results showed that sucralose ingestion yielded an increase in peak plasma glucose concentration, peak plasma insulin, and C-peptide concentrations while it decreased insulin clearance rate. GLP-1 and GIP concentrations, as well as β-cell sensitivity were not significantly different after sucralose or water ingestion.
In conclusion, the ingestion of sucralose alters the metabolic response to an oral glucose load in obese patients who are not regular consumers of nonnutritive sweeteners.
This study supports the concept that artificial sweeteners are not metabolically inert, and can potentially serve a purpose in the diet of those that do not normally consume artificial sweeteners in their everyday diet. Additional studies should be performed to establish their effectiveness in children, chronic nonnutritive sweetener users in obese patients, as well as ethnically diverse patient populations.
- The gastrointestinal tract and the pancreas can detect sugars through taste receptors that are similar to those found in the taste cells of the mouth.
- Activation of sweet taste receptors in the gut by nonnutritive sweeteners can trigger the secretion of glucagon-like peptide 1 (GLP-1) and insulin.
Pepino, M. Y. et al. "Sucralose Affects Glycemic and Hormonal Responses to an Oral Glucose Load." Diabetes Care 36 (2013): 2530-535.