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Interactions between bitter taste, diet and dysbiosis: Consequences for appetite and obesity

Abstract

The type 2 family of taste receptors (T2Rs) detect and respond to bitter tastants. These receptors are expressed throughout the gastrointestinal (GI) tract, with location dependant roles. In the oral cavity, T2Rs are involved in the conscious perception of bitter tastants, while in the lower GI tract they have roles in chemoreception and regulation of GI function. Through these diverse roles, these receptors may be involved in modulating appetite and diet, with consequences for weight regulation and obesity. Interestingly, the concentration of T2Rs in the GI tract is greatest in the large intestine, the organ with the densest colonisation of bacteria. The gut microbiome has been the subject of intense research, as a plethora of roles linking microbiota to human health continue to be uncovered. Of particular interest is the microbial signature associated with obesity. Obesity is a leading health concern, and advances in our understanding of this disease are needed. Diet is a known modifiable factor in the development of obesity. However, diet only partially explains disease risk. Changes in microbial energy harvesting by the microbiota plays a role in obesity, and the composition of these energy harvesting populations may be controlled by taste receptors. This review explores T2Rs as a potential link between obesity and the human GI microbiome.

Journal Article Type Article
Publication Date Sep 20, 2018
Journal Nutrients
Print ISSN 2072-6643
Publisher MDPI
Peer Reviewed Peer Reviewed
Volume 10
Issue 10
Article Number 1336
APA6 Citation Turner, A., Veysey, M., Keely, S., Scarlett, C., Lucock, M., & Beckett, E. (2018). Interactions between bitter taste, diet and dysbiosis: Consequences for appetite and obesity. Nutrients, 10(10), https://doi.org/10.3390/nu10101336
DOI https://doi.org/10.3390/nu10101336
Keywords T2R; TAS2R; Bitter; Dysbiosis; Microbiota; Obesity; Microbiome; Diet
Publisher URL https://www.mdpi.com/2072-6643/10/10/1336

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Copyright Statement
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).





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