Figure 2.

Overview of the mechanisms of how artificial sweeteners may affect physiological processes involved in body weight regulation. Artificial sweeteners interact with T1R-family of sweet-taste receptors in the oral cavity and gastrointestinal tract, thereby able to affect satiety and, in turn, energy intake and body weight. However, in vivo studies have shown no effect of artificial sweeteners on the secretion of incretins. Furthermore, several artificial sweeteners may reach the adipose tissue to interact with T1R-family of sweet-taste receptors and affect adipogenesis and, in turn, body weight. Moreover, several artificial sweeteners are able to induce gut microbiota alterations. Thereupon, SCFA production is enhanced. It can be speculated that SCFA may, in turn, increase energy expenditure due to enhanced lipid oxidation and affect satiety by modulating gut-brain signaling via incretins. Dashed lines indicate that the effect is dependent on type of artificial sweetener and/or that results are inconsistent or hypothetical. SCFA, short chain fatty acids; GPCR; G-protein coupled receptor; T1R2, taste receptor type 1 member 2; T1R3, taste receptor type 1 member 3.