Endocrine Abstracts

Background: Obesity is a disease with disastrous health, social and economic consequence. There is presently a global epidemic of obesity in all age groups and in both developed and developing countries. Understanding the nutrient and chemical sensing mechanisms in the gastro-intestinal tract (GIT) which act to trigger gut hormone release and appetite after food consumption is crucial to be able to devise effective methods to reduce and prevent obesity. Recently, the sweet taste receptor (T1r2+T1r3) has been found to be expressed in endocrine L-cells throughout the GIT. Application of sucralose (a non-calorific, non-metabolisable sweetener) to L-cells in vitro stimulates GLP-1 secretion, an effect that is inhibited with co-administration of lactisole, a T1r2+T1r3 inhibitor.

Objective: We conducted a randomised-controlled trial in eight healthy volunteers to investigate whether ingestion of sucralose could stimulate GLP-1 and PYY release in healthy volunteers.

Design: The study was conducted with local Ethical Committee approval. Following a 12 h fast, subjects consumed 50 ml of either water, sucralose (0.083% w/v) or a non-sweet, glucose-polymer matched for sweetness (50% maltodextrin+0.083% sucralose) in a randomised order on separate study days, at least 3 days. Appetite ratings and blood samples were taken for 2 h and caloric intake was measured at lunch. Plasma GLP-1, PYY, insulin and glucose were calculated as incremental area under the curve (iAUC).

Results: Sucralose ingestion had similar effects to water ingestion and did not increase plasma GLP-1 (−358.6±401.3 vs −675.0±1609.9 respectively) or PYY (−56.08±192.3 vs −179.3±119.4). Maltodextrin significantly increased insulin and glucose compared to water (P<0.001) and showed a non-significant trend towards increased PYY and GLP-1. Appetite ratings and food intake were similar for all groups.

Conclusion: At this dose the non-calorific, non-metabolisable sweetener Sucralose does not stimulate a detectable plasma GLP-1 or PYY rise and does not reduce appetite in healthy volunteers.