Experience with the high-intensity sweetener saccharin impairs glucose homeostasis and GLP-1 release in rats

Abstract

Previous work from our lab has demonstrated that experience with high-intensity sweeteners in rats leads to increased food intake, body weight gain and adiposity, along with diminished caloric compensation and decreased thermic effect of food. These changes may occur as a result of interfering with learned relations between the sweet taste of food and the caloric or nutritive consequences of consuming those foods. The present experiments determined whether experience with the high-intensity sweetener saccharin versus the caloric sweetener glucose affected blood glucose homeostasis. The results demonstrated that during oral glucose tolerance tests, blood glucose levels were more elevated in animals that had previously consumed the saccharin-sweetened supplements. In contrast, during glucose tolerance tests when a glucose solution was delivered directly into the stomach, no differences in blood glucose levels between the groups were observed. Differences in oral glucose tolerance responses were not accompanied by differences in insulin release; insulin release was similar in animals previously exposed to saccharin and those previously exposed to glucose. However, release of GLP-1 in response to an oral glucose tolerance test, but not to glucose tolerance tests delivered by gavage, was significantly lower in saccharin-exposed animals compared to glucose-exposed animals. Differences in both blood glucose and GLP-1 release in saccharin animals were rapid and transient, and suggest that one mechanism by which exposure to high-intensity sweeteners that interfere with a predictive relation between sweet tastes and calories may impair energy balance is by suppressing GLP-1 release, which could alter glucose homeostasis and reduce satiety.

The effect of moderate consumption of non-nutritive sweeteners on glucose tolerance and body composition in rats

“…However, when the glucose load was given by gavage bypassing the oral taste receptors, as in this study, a normal response to the glucose load was observed (Swithers et al 2012). Conversely, glucose AUC was higher in response to an intraperitoneal glucose load in high-fat fed mice (Gul et al 2017) and in mice with dietary-induced obesity (Mitsutomi et al 2014) treated with aspartame.…”

“…A hyperglycemic response to an oral glucose load was found when NNS were delivered in the diet (Swithers et al 2012), or drinking water (Suez et al 2014;Palmnas et al 2014;Mitsutomi et al 2014;Gul et al 2017) indicating a disconnect between the sweet taste and the learned response to control energy balance. However, when the glucose load was given by gavage bypassing the oral taste receptors, as in this study, a normal response to the glucose load was observed (Swithers et al 2012).…”

Non-caloric artificial sweeteners and the microbiome: findings and challenges

“…Rats consuming sucralose were also shown by Schiffman and colleagues 26 to gain more weight, a finding that initiated intense debate. 27 In addition to weight gain, both saccharin and aspartame have been associated with impaired glucose homeostasis in mice, 24,28,29 and aspartame was also shown to induce hyperinsulinemia, 25 impaired insulin tolerance 24,28 and worsened atherosclerosis in genetically-susceptible (ApoE ¡/¡ ) mice. 30,31 In contrast, Flatt and colleagues described anti-hyperglycemic and antihyperinsulinemic effects for saccharin in genetically obese (ob/ob) mice, coupled with attenuation of weight gain.…”

A Review on Dhatryadi Ghrita

“…Increased glucose utilization in the liver and peripheral tissues was causing the transient hypoglycemic effect due to the complex polysaccharides present in the Sugarcane. 16 …”