> The upper gastrointestinal tract is well-endowed with taste and fat receptors, with sweet taste being detected, as elsewhere, by a heterodimer of the taste 1 receptor (T1R) family, T1R2/T1R3. These receptors have been localized to intestinal brush and enteroendocrine cells, and are coupled with α-gustducin as the α-subunit of the G protein (Fig. 1). They recognize sugars, d-amino acids, sweet proteins, and artificial sweeteners. Of importance to a possible role in the incretin response, these receptors are colocalized with glucagon-like peptide 1 (GLP-1) and L cells containing peptide YY (PYY) and K cells containing glucose-dependent insulinotropic polypeptide (GIP) (3). Incidentally, fatty acid responsive GPRs are also coupled to GLP-1 release, but are found predominantly in the colon (5).
Can be restated in plain English: Cells in the GI tract between one's mouth and duodenum have similar sweet taste receptors - T1R. Some of these cells are endocrine and store GLP-1, PYY, and GIP (incretin) messenger hormones.
For context, messenger hormones cause changes in cells receptive to them, including the nervous system. Indirectly, these hormones can affect metabolism and feeling of hunger or fullness (this is not in the paper but is known).
The paper then discusses inconsistent (but meaningful) evidence for sweet taste receptors influencing the messenger hormone release and insulin-glycemia response. Notably, the author suggests sucralose sweeteners consumed before carbohydrates might spike postprandial (after-meal) blood sugar and insulin response. However, the extent of this effect could depend on an individual's genetics. The link between messenger hormone release and sweet taste receptors is established because this effect is diminished in vivo in mice lacking specific sweet taste receptors.