Effect of the artificial sweetener, sucralose, on small intestinal glucose absorption in healthy human subjects

Abstract

It has been reported that the artificial sweetener, sucralose, stimulates glucose absorption in rodents by enhancing apical availability of the transporter GLUT2. We evaluated whether exposure of the proximal small intestine to sucralose affects glucose absorption and/or the glycaemic response to an intraduodenal (ID) glucose infusion in healthy human subjects. Ten healthy subjects were studied on two separate occasions in a single-blind, randomised order. Each subject received an ID infusion of sucralose (4 mM in 0·9 % saline) or control (0·9 % saline) at 4 ml/min for 150 min (T ¼ 230 to 120 min). After 30 min (T ¼ 0), glucose (25 %) and its non-metabolised analogue, 3-O-methylglucose (3-OMG; 2·5 %), were co-infused intraduodenally (T ¼ 0 -120 min; 4·2 kJ/min (1 kcal/min)). Blood was sampled at frequent intervals. Blood glucose, plasma glucagonlike peptide-1 (GLP-1) and serum 3-OMG concentrations increased during ID glucose/3-OMG infusion (P,0·005 for each). However, there were no differences in blood glucose, plasma GLP-1 or serum 3-OMG concentrations between sucralose and control infusions. In conclusion, sucralose does not appear to modify the rate of glucose absorption or the glycaemic or incretin response to ID glucose infusion when given acutely in healthy human subjects.3-O-methylglucose: Sodium-dependent GLUT 1: GLUT 2: Glucagon-like peptide-1The mechanisms by which the gut senses nutrients are unclear, and the 'receptor' for detecting luminal carbohydrates has, until recently, been elusive. Recent studies indicate the presence of G-protein-coupled taste receptors, T1R2 and T1R3, and their taste signal transduction partners, the G-protein gustducin and the transient receptor potential ion channel TRPM5, in the mucosa of the mouse and human gastrointestinal tract (1,2) . These receptors, analogous to sweet taste receptors on the tongue, broadly respond to sugars and artificial sweeteners, and among several cell types, they appear to co-localise with glucagon-like peptide-1 (GLP-1)-secreting L cells (3) .It has been reported that the artificial sweetener, sucralose, stimulates the secretion of both GLP-1 and glucose-dependent insulinotrophic polypeptide from the mouse enteroendocrine cell line GLUTag (4) , and it stimulates GLP-1 secretion from the human L cell line NCI-H716 (3) , a response that is blocked by the sweet receptor antagonist, lactisole, and siRNA for a-gustducin (3) . However, we recently demonstrated that sucralose, in two different loads, had no effect on GLP-1, glucose-dependent insulinotrophic polypeptide or insulin secretion, and that it did not elicit any feedback response on gastric emptying in healthy human subjects (5) . While this implies that artificial sweeteners may have no therapeutic benefit in the dietary management of diabetes, other than as a substitute for carbohydrates, it remains possible that sucralose affects small intestinal carbohydrate absorption as a result of its interaction with the sweet taste receptors.Glucose is absorbed from the small intestine through both ...

Biological Effect of Sucralose in Diabetic Rats

“…Supporting our postulation Abou-Donia et al [21] reported that the administration of sucralose at 1.1 -11 mg/kg to male rats for 12-week's interfere with the absorption of nutrients and drugs. However, contrarily to our results, in vitro study revealed that sucralose induces insulin secretion by Ca 2+ and cAMP-dependent mechanisms [37] and has no effect on the rate of glucose absorption [38]. Moreover, studies on diabetic patients (Type 1 and type 2) showed that the administration of 1000 mg sucralose had no effect on plasma glucose [39], as well as, the administration of 7.5 mg/kg/day sucralose during 3-months' had no effect on glycated hemoglobin, and fasting plasma glucose in individuals with type 2 diabetes [40].…”

Consumption of non-nutritive sweeteners and nutritional status in 10-16 year old students

“…29 In addition, when sucralose, aspartame or acesulfame k are delivered intraduodenally, they do not have an effect on postprandial blood glucose levels, GLP-1 secretion or glucose absorption by the small intestine lumen. 30,31 To date, only this last mechanism has been studied in humans. Data on humans and animals are contradictory, and it is not clear if NNS affect incretin response (GLP-1 and GIP) in vivo by means of the interaction of intestinal receptors for sweet taste.…”

“…Data on humans and animals are contradictory, and it is not clear if NNS affect incretin response (GLP-1 and GIP) in vivo by means of the interaction of intestinal receptors for sweet taste. 30,31 Some of this study's strengths are that using the frequency consumption survey provided information on the usual NNS intake among surveyed students and that the set of pictures allowed respondents to identify the corresponding NNS-containing foods. Some of this study's weaknesses are that the survey tends to overestimate intake and is based on respondents' recall, that it is difficult to establish serving sizes and, above all, that this is a cross-sectional study…”

A randomized control trial for reduction of caloric and non-caloric sweetened beverages in young adults: effects in weight, body composition and blood pressure

“…It has been proposed that the shift from the consumption of plain water to sugar-sweetened beverages is associated with the increase of obesity frequency (7). Because the diminished sensation of satiety and the high ingestion of sugar (8) facilitate the formation of triglycerides stored in fatty tissue and overweight and obesity (9,10).…”