Plain language summary
Artificial sweeteners have been used to replace carbohydrate in the management of diabetes and obesity. Sucralose is a noncaloric sweetener derived from sucrose and is ∼600 times sweeter. The aims of this study were to evaluate the incretin [metabolic hormone], insulin, and glycaemic responses to sucralose administration and to determine whether this artificial sweetener is capable of generating feedback in the small intestine that slows gastric emptying in healthy humans. This study studied seven healthy subjects whose average age was 24 years. Each subject attended the Discipline of Medicine at the Royal Adelaide Hospital on four occasions (after 14hr overnight fast), each separated by 3–7 days. Women were studied in the follicular phase of the menstrual cycle. Results indicate that fasting blood glucose concentrations and plasma incretin and insulin concentrations did not differ between the four study days. Authors conclude that artificial sweeteners may have no therapeutic benefit in the dietary management of diabetes, other than as a substitute for carbohydrate.
Abstract
The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in glucose homeostasis in both health and diabetes. In mice, sucralose, an artificial sweetener, stimulates GLP-1 release via sweet taste receptors on enteroendocrine cells. We studied blood glucose, plasma levels of insulin, GLP-1, and GIP, and gastric emptying (by a breath test) in 7 healthy humans after intragastric infusions of 1) 50 g sucrose in water to a total volume of 500 ml (approximately 290 mosmol/l), 2) 80 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 0.4 mM sucralose), 3) 800 mg sucralose in 500 ml normal saline (approximately 300 mosmol/l, 4 mM sucralose), and 4) 500 ml normal saline (approximately 300 mosmol/l), all labeled with 150 mg 13C-acetate. Blood glucose increased only in response to sucrose (P<0.05). GLP-1, GIP, and insulin also increased after sucrose (P=0.0001) but not after either load of sucralose or saline. Gastric emptying of sucrose was slower than that of saline (t50: 87.4+/-4.1 min vs. 74.7+/-3.2 min, P<0.005), whereas there were no differences in t50 between sucralose 0.4 mM (73.7+/-3.1 min) or 4 mM (76.7+/-3.1 min) and saline. We conclude that sucralose, delivered by intragastric infusion, does not stimulate insulin, GLP-1, or GIP release or slow gastric emptying in healthy humans.
Methodological quality
Jadad score
:
Not applicable
Allocation concealment
:
Not applicable
