The Combined Effects of Aspartame and Acesulfame-K Blends on Appetite: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.

Aspartame (Asp) and acesulfame-K (Ace-K) are nonnutritive sweeteners (NNSs) commonly used in combination to replace added sugars in reduced- or low-calorie foods and beverages. Despite Asp/Ace-K blends having negligible calories, their effects on appetite have not been reviewed systematically. We therefore undertook a systematic review and meta-analysis of the metabolic effects of Asp/Ace-K blends on energy intake (EI), subjective appetite scores, blood glucose, and the incretin hormones glucose-dependent insulinotropic peptide and glucagon-like peptide.

Evolution of complex, discreet nutrient sensing pathways.

Purpose Of Review: The current review summarizes and discusses current research on differences elicited between sugars and nonnutritive sweeteners via sugar-sensing pathways.

Recent Findings: Sugars, sweeteners, and sweetening agents are all perceived as sweet tasting because of their ability to bind to the type 1 taste receptor family of sweet taste receptors in the oral cavity. The ability of a wide variety of chemical ligands to activate the sweet taste receptor highlights the importance of sweet-tasting foods during human evolution.

Correction: Acute Effects of Sugars and Artificial Sweeteners on Small Intestinal Sugar Transport: A Study Using CaCo-2 Cells As an In Vitro Model of the Human Enterocyte.

[This corrects the article DOI: 10.1371/journal.pone.

Acute Effects of Sugars and Artificial Sweeteners on Small Intestinal Sugar Transport: A Study Using CaCo-2 Cells As an In Vitro Model of the Human Enterocyte.

Background: The gastrointestinal tract is responsible for the assimilation of nutrients and plays a key role in the regulation of nutrient metabolism and energy balance. The molecular mechanisms by which intestinal sugar transport are regulated are controversial. Based on rodent studies, two models currently exist that involve activation of the sweet-taste receptor, T1R2/3: an indirect model, whereby luminal carbohydrates activate T1R2/3 expressed on enteroendocrine cells, resulting in the release of gut peptides which in turn regulate enterocyte sugar transport capacity; and a direct model, whereby T1R2/3 expressed on the enterocyte regulates enterocyte function.