Non-nutritive sweeteners can bind to sweet-taste receptors present not only in the oral cavity, but also on enteroendocrine and pancreatic islet cells. Thus, these sweeteners may have biological activity by eliciting or inhibiting hormone secretion. Because consumption of non-nutritive sweeteners is common in the United States, understanding the physiological effects of these substances is of interest and importance.
A PubMed (1960-2012) search was performed to identify articles examining the effects of non-nutritive sweeteners on gastrointestinal physiology and hormone secretion.
The majority of in vitro studies showed that non-nutritive sweeteners can elicit secretion of gut hormones such as glucagon-like peptide 1 and glucose-dependent insulinotropic peptide in enteroendocrine or islet cells. In rodents, non-nutritive sweeteners increased the rate of intestinal glucose absorption, but did not alter gut hormone secretion in the absence of glucose. Most studies in humans have not detected effects of non-nutritive sweeteners on gut hormones or glucose absorption. Of eight human studies, one showed increased glucose-stimulated glucagon-like peptide 1 secretion after diet soda consumption, and one showed decreased glucagon secretion after stevia ingestion.
In humans, few studies have examined the hormonal effects of non-nutritive sweeteners, and inconsistent results have been reported, with the majority not recapitulating in vitro data. Further research is needed to determine whether non-nutritive sweeteners have physiologically significant biological activity in humans.
"The relevance of the findings from studies conducted in cell systems and rodent models to human physiology is not clear because the NNS data obtained from studies conducted in people often fail to replicate the metabolic outcomes observed in vitro and in animal models (rev. in 13). The results from most (14–18), but not all (19,20), studies conducted in people have found that NNS do not affect plasma glucose, insulin, or GLP-1. "
[Show abstract][Hide abstract] ABSTRACT: OBJECTIVE
Nonnutritive sweeteners (NNS), such as sucralose, have been reported to have metabolic effects in animal models. However, the relevance of these findings to human subjects is not clear. We evaluated the acute effects of sucralose ingestion on the metabolic response to an oral glucose load in obese subjects.RESEARCH DESIGN AND METHODS
Seventeen obese subjects (BMI 42.3 ± 1.6 kg/m(2)) who did not use NNS and were insulin sensitive (based on a homeostasis model assessment of insulin resistance score ≤2.6) underwent a 5-h modified oral glucose tolerance test on two separate occasions preceded by consuming either sucralose (experimental condition) or water (control condition) 10 min before the glucose load in a randomized crossover design. Indices of β-cell function, insulin sensitivity (SI), and insulin clearance rates were estimated by using minimal models of glucose, insulin, and C-peptide kinetics.RESULTSCompared with the control condition, sucralose ingestion caused 1) a greater incremental increase in peak plasma glucose concentrations (4.2 ± 0.2 vs. 4.8 ± 0.3 mmol/L; P = 0.03), 2) a 20 ± 8% greater incremental increase in insulin area under the curve (AUC) (P < 0.03), 3) a 22 ± 7% greater peak insulin secretion rate (P < 0.02), 4) a 7 ± 4% decrease in insulin clearance (P = 0.04), and 5) a 23 ± 20% decrease in SI (P = 0.01). There were no significant differences between conditions in active glucagon-like peptide 1, glucose-dependent insulinotropic polypeptide, glucagon incremental AUC, or indices of the sensitivity of the β-cell response to glucose.CONCLUSIONS
These data demonstrate that sucralose affects the glycemic and insulin responses to an oral glucose load in obese people who do not normally consume NNS.
Diabetes care 04/2013; 36(9). DOI:10.2337/dc12-2221 · 8.42 Impact Factor
"Dietary sugars and nonnutritive sweeteners are primarily sensed by the sweet taste receptor, a GPCR that is functionally present as the heterodimer T1R2+T1R3 in taste buds within the oral cavity of most mammals (Treesukosol et al., 2011). This receptor is also expressed in distal parts of the GI tract, where its activation by glucose and noncaloric sweeteners may stimulate the secretion of GLP-1 and other gut peptides in pigs (Shirazi-Beechey et al., 2011; Mace and Marshall, 2012); however, a number of studies with rodents and humans were unable to confi rm such a response (Brown and Rother, 2012). The inconsistent results encourage further research to evaluate the potential role of agonists of the porcine T1R2+T1R3 in promoting or sustaining intestinal growth at weaning. "
[Show abstract][Hide abstract] ABSTRACT: Pig production is a commodity business, which makes it a cost-driven business. Pig producers and their advisors are appropriately reluctant to adopt technologies without confidence that improved production will more than pay for the cost of the technology. Physiological effects of technologies targeting gut sensory pathways must translate to demonstrably improved health and(or) productive performance if they are to be adopted. The types and degrees of stressors experienced by pigs in commercial production vary widely, and often differ from those in research herds, and those variations influence their productive responses to nutritional and health technologies. Pigs are most vulnerable to disease soon after weaning, and the diets fed to pigs at that time are more expensive and offered in much smaller amounts than those fed later in life. Those factors make it easier to justify expensive dietary technologies for young pigs than for older ones. New developments in gut chemosensing appear important, but their practical application is not yet clear. We suggest investigation of the potential to connect chemical detection by the gut to pig productivity and(or) efficiency through the following mechanisms: 1) trophic effects on the intestines, which lead to improved enteric health or enhanced nutrient digestion and absorption; 2) enhanced barrier function in the intestinal mucosa; 3) increased feed intake; 4) enhanced insulin secretion and sensitivity, which may be especially useful in lactating sows to improve subsequent reproduction; and 5) other signals triggered by products of enteric fermentation, possibly short-chain fatty acids, that may influence gut integrity, feed intake, and reproductive function. Each of these mechanisms relates to a practical issue in pig production. Practical application would likely be achieved through dietary changes, but separate management factors, drugs, or other interventions may also be developed.
[Show abstract][Hide abstract] ABSTRACT: Insulin secretion from pancreatic β cells is controlled by nutrients, hormones, and neurotransmitters. Unlike the latter, which work through classic receptors, glucose and most other nutrients do not interact with membrane receptors but must be metabolized by β cells to induce insulin secretion. Studies have revealed the presence of umami and sweet taste receptors and their downstream effectors in β cells. That the receptors are functional was established by the effects of fructose and artificial sweeteners, which induced signals similar to those produced in taste buds of the tongue. These signals mediated an increase in insulin secretion in the presence of glucose. However, the physiological implications of these pathways in insulin secretion are unclear because of the large differences between plasma concentrations of fructose or sweeteners and their effective concentrations in vitro.
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