Low calorie sweeteners: Evidence remains lacking for effects on human gut function

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Autor(en) : Bryant C., McLaughlin J
Name der Veröffentlichung : Physiol Behav 2016 Oct 1;164(Pt B):482-5
Erscheinungsjahr : 2016


The importance of nutrient induced gut-brain signalling in the regulation of human food intake has become an increasing focus of research. Much of the caloric excess consumed comes from dietary sugars, but our knowledge about the mechanisms mediating the physiological and appetitive effects of sweet tastants in the human gut and gut-brain axis is far from complete. The comparative effects of natural sugars vs low calorie sweeteners are also poorly understood. Research in animal and cellular models has suggested a key functional role in gut endocrine cells for the sweet taste receptors previously well described in oral taste. However human studies to date have very consistently failed to show that activation of the sweet taste receptor by low calorie sweeteners placed in the human gut fails to replicate any of the effects on gastric motility, gut hormones or appetitive responses evoked by caloric sugars.


The scientific review by Bryant and McLaughlin has found that there is a lack of evidence for effects of low calorie sweeteners (LCS) on gut function. The review covers cellular, animal and clinical studies and puts the results of this research into context with regard to the gut-brain axis and its regulation of food intake, and was conducted in light of recent hypotheses suggesting an effect of LCS on human health via activation of gut taste receptors and/or release of gut hormones involved in nutrient signaling and appetite regulation.

After reviewing the collective evidence, the authors concluded that available human studies do not support a clinically meaningful effect of LCS on gut hormones that are involved in either blood glucose or appetite control. Based on the scientific evidence, they found that sucralose, aspartame and ace-K had no greater effect than water on secretion of GLP-1, insulin, PYY or ghrelin, nor any impact on appetitive responses.

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