The Sweet Taste Signalling Pathways

Int J Food Sci Nutr. 2018 Jul 30:1-11. doi: 10.1080/09637486.2018.1492522.
Han P, Bagenna B, Fu M.


  • To review the current evidence regarding physiological responses relevant to sweet taste mechanisms and the impact on appetite control.
  • Specifically, the review focuses on the type 1 member 2 (T1R2)/ type 1 member 3 (T1R3) subunits of taste receptors in the oral cavity and the gastrointestinal tract (GIT), which are activated by sugars, D-amino acids, sweet proteins and non-nutritive sweeteners (NNS).
  • The relationship among sweet agonists, appetite and food intake was also summarized.


  • Sweet taste has been associated with food reward and carbohydrate energy sources. However, excessive sugar consumption is blamed for the prevalence of overweight and obesity.
  • To expand the understanding of sweet agonists in appetite, satiety and food intake, it is important to understand the physiological and neural responses to sweet taste agonists-receptor bindings at various sites during food consumption, mainly the oral cavity and GIT. In addition, it is important to understand the similarity and differences between the effect of caloric sugar and NNSs.
  • Currently, it is known that not all sweeteners bind to the same sites on the taste receptors. Common caloric sweeteners, including sucrose, fructose and sucralose, certain NNSs like saccharin and Acesulfame-K, and dipeptide sweeteners such as aspartame and neotame, preferentially bind to sites on T1R2. Cyclamate, however, binds to T1R3.


  • Peer-reviewed publications written in English were searched in PubMed, Google Scholar and Web of Science. Those covering either caloric sugar or NNS on the following topics were screened and reviewed:
    • Hormonal and/or brain responses to sweet taste agonists presented in oral cavity or GIT;
    • Sweet taste perception, satiety and food intake.
  • The main findings of included articles were synthesized and compared between caloric sugars and NNSs. The majority of reviewed studies included human participants, except for those investigating GIT administration of sweet agonists and hormonal responses and brain activation. This was due to the lack of data for human participants.
  • The investigators reviewed hormonal response to oral and GIT perception of sweetness (cephalic phase responses), as well as brain responses to sweetness via oral or GIT administration. Lastly, the relationship between sweet perception, satiety and food intake in humans was discussed, highlighting the importance of individual sweetness perceptual variations.


  • The studies reviewed showed mixed findings on the cephalic phase hormone response to sugar and NNSs in human subjects.   
  • To date there are no human neuroimaging studies that explore the direct effects of gut stimulation by sugar or NNSs on the brain.  Animal studies indicated that brain response induced by sweet sensing in the GIT is similar to that in the oral cavity.
  • Study findings consistently showed no impact of NNS on gastric emptying, appetite sensations, or hormone secretions in humans.
  • The results of investigations of the association between sweet sensitivity and food intake were mixed. Discrepancies between studies were likely due to differences in study participants and sweet taste sensitivity and dietary intake assessment methods.


  • Compared to NNSs, caloric sugars have a stronger potency in regulating hormone secretion and brain activation of the reward circuitry relevant for appetite control.
  • The evidence summarized in this report suggest that NNSs may serve as a good substitute for sugar to provide sweet taste with little energy.
  • The long term effect of caloric sugars and NNS on the regulation of appetite and food intake in humans remains unclear and will require further investigation.
  • Future studies need to better control the condition of both subjects and stimulus and account for individual differences regarding CPIR. Mixed or missing information regarding the stimuli, including the concentration and duration of the sweet stimulus, make direct comparisons between studies difficult.

Points to Consider

  • The failure of NNS to elicit the release of peptides associated with gastric emptying, appetite sensations and hormone secretions could theoretically result in lower satiety and augmented energy intake.
  • While sweet taste seems to not have an impact on satiety, inter-individual variations of sweet perceptions were related to food choice and consumption.

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