Sweet Taste Antagonist Lactisole Administered in Combination with Sucrose, But Not Glucose, Increases Energy Intake and Decreases Peripheral Serotonin in Male Subjects.

Kerstin Schweiger,Corinna M Karl,Gerhard E Krammer,Verena Grüneis,Julia Treml,Veronika Somoza,Claudia Galassi,Jakob P Ley,Barbara Lieder

doi:10.3390/nu12103133

Abstract

Knowledge regarding the involvement of sweetness perception on energy intake is scarce. Here, the impact of glucose and sucrose sweetness, beyond their caloric load, on subsequent food intake and biomarkers of satiation was evaluated by co-administration of the sweet taste receptor inhibitor lactisole. A total of 27 healthy, male subjects received solutions of either 10% glucose w/o 60 ppm lactisole or 10% sucrose w/o 60 ppm lactisole. Subsequent food intake from a standardized breakfast was evaluated 2 h after receiving the respective test solution. Changes in postprandial plasma concentrations of cholecystokinin, ghrelin, and serotonin were determined over a period of 120 min, as was the body temperature. Administration of lactisole to the sucrose solution increased the energy intake from the subsequent standardized breakfast by 12.9 ± 5.8% (p = 0.04), led to a decreased Δ AUC of the body core temperature by 46 ± 20% (p = 0.01), and time-dependently reduced Δ serotonin plasma concentrations (−16.9 ± 6.06 ng/mL vs. −0.56 ± 3.7 ng/mL after sucrose administration, p = 0.03). The present study shows that lactisole increases energy intake and decreases plasma serotonin concentrations as well as body core temperature induced by sucrose, but not glucose. This finding may be associated with the different binding affinities of sucrose and glucose to the sweet taste receptor.

Highlights

Sweet taste is discussed as a predicting factor for subsequent food consumption [1,2,3]
Sweetness perception is mediated by the canonical sweet taste receptor, a heterodimeric G-protein coupled receptor consisting of the two subunits T1R2 and T1R3, of which T1R3 is selectively targeted by Nutrients 2020, 12, 3133; doi:10.3390/nu12103133
We investigated the impact of lactisole, a T1R3 antagonist, on short-term energy intake and release of satiety hormones induced by glucose or sucrose administered to healthy subjects in concentrations corresponding to a regular soft drink

Summary

Introduction

Sweet taste is discussed as a predicting factor for subsequent food consumption [1,2,3]. With a stimulation of the sweet taste receptor, the G-protein subunit α-gustducin leads to an activation of gustatory nerve fibers through a signal transduction pathway, transmitting the information to the brain via the central nervous system [7]. T1R2/T1R3 chemoreceptors are present in the oral cavity and in extraoral tissues, such as the gastrointestinal tract [8,9], and are thought to be involved in physiological responses to nutrients, like sugar sensing, glucose homeostasis, and the secretion of satiety hormones, thereby contributing to maintain energy balance [10,11]. The control of food intake is pivotal to energy balance and regulated by the sensation of satiation and satiety. Whereas satiety is defined as the feeling of fullness that persists after finishing a meal, satiation leads to the termination of eating [12]

Methods

Results

Discussion

Conclusion