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Non-nutritive sweeteners, energy balance, and glucose homeostasis

Pepino, Marta Y; Bourne, Christina

Current Opinion in Clinical Nutrition & Metabolic Care: July 2011 - Volume 14 - Issue 4 - p 391–395
doi: 10.1097/MCO.0b013e3283468e7e
Carbohydrates: Edited by Luc Tappy and Bettina Mittendorfer

Purpose of review To review the recent work on potential mechanisms underlying a paradoxical positive association between the consumption of non-nutritive sweeteners (NNS) and weight gain.

Recent findings Several potential mechanisms, not mutually exclusive, are hypothesized. First, by dissociating sweetness from calories, NNS could interfere with physiological responses that control homeostasis. Second, by changing the intestinal environment, NNS could affect the microbiota and in turn trigger inflammatory processes that are associated with metabolic disorders. Third, by interacting with novel sweet-taste receptors discovered in the gut, NNS could affect glucose absorptive capacity and glucose homeostasis. The latter mechanism that has received the most attention recently. Some animal studies, but not all, found that NNS activate gut sweet-taste pathways that control incretin release and upregulate glucose transporters. Human studies found that, at least for healthy fasted individuals, the sole interaction of NNS with sweet-taste gut receptors is insufficient to elicit incretin responses. The reasons for discrepancy between different studies are unknown but could be related to the species of mammal tested and the dose of NNS used.

Summary Whether NNS are metabolically inactive, as previously assumed, is unclear. Further research on the potential effects of NNS on human metabolism is warranted.

School of Medicine, Washington University in St. Louis, St. Louis, Missouri, USA

Correspondence to Marta Y. Pepino, PhD, Research Assistant Professor, School of Medicine, Washington University in St. Louis, 660 South Euclid Avenue, St. Louis, MO 63110, USA Tel: +1 314 362 8113; fax: +1 314 362 8230; e-mail:

© 2011 Lippincott Williams & Wilkins, Inc.