Human taste detection of glucose oligomers with low degree of polymerization

Abstract

Studies have reported that some animals, including humans, can taste mixtures of glucose oligomers (i.e., maltooligosaccharides, MOS) and that their detection is independent of the known T1R2/T1R3 sweet taste receptor. In an effort to understand potential mechanisms underlying the taste perception of glucose oligomers in humans, this study was designed to investigate: 1) the variability of taste sensitivity to MOS with low degree-of-polymerization (DP), and 2) the potential role of hT1R2/T1R3 in the MOS taste detection. To address these objectives, a series of food grade, narrow-DP-range MOS were first prepared (DP 3, 3–4, 5–6, and 6–7) by fractionating disperse saccharide mixtures. Subjects were then asked to discriminate these MOS stimuli as well as glucose (DP 1) and maltose (DP 2) from blanks after the stimuli were swabbed on the tongue. All stimuli were presented at 75 mM with and without a sweet taste inhibitor (lactisole). An α-glucosidase inhibitor (acarbose) was added to all test stimuli to prevent oral digestion of glucose oligomers. Results showed that all six stimuli were detected with similar discriminability in normal tasting conditions. When the sweet receptor was inhibited, DP 1, 2, and 3 were not discriminated from blanks. In contrast, three higher-DP paired MOS stimuli (DP 3–4, 5–6, and 6–7) were discriminated from blanks at a similar degree. Overall, these results support the presence of a sweet-independent taste perception mechanism that is stimulated by MOS greater than three units.

An alternative pathway for sweet sensation: possible mechanisms and physiological relevance

“…As mentioned earlier, preference and nerve responsiveness to disaccharides and polycose were largely unaltered in T1R3knockout mice [325,326,357]. Consistently, sensation of disaccharides [56,355] and malto-oligosaccharides in humans appears to be sweet-taste receptor-independent [154,155,232]. Decomposition of starch, a major plant polysaccharide, involves oral salivary amylases followed by pancreatic amylase in the small intestine [239].…”

“…Concerning polysaccharides, several lines of evidence suggest that they employ a sweet-taste receptor-independent pathway [154,155,232,326]. First, sucrose and oligosaccharide intake were differentially affected by gustatory-nerve transection in rat: while chorda-tympani transection altered the consumption of both, sucrose and polycose, glossopharyngeal transection selectively reduced polycose intake [331].…”

Gut Mechanisms Linking Intestinal Sweet Sensing to Glycemic Control

“…Importantly, mice lacking one or both STR subunits had limited, or no behavioral or lingual nerve responses to simple sugars, while responses to polycose remained normal (124–127). More recently, behavioral research on human taste detection have added support for a human polycose taste receptor, showing that humans can detect glucose oligomer solutions on an equimolar basis to simple sugars, even when lingual STR were blocked with lactisole and amylase activity inhibited by an α-glucosidase inhibitor (to prevent oral breakdown of glucose oligomers to STR-detectable mono- and disaccharides) (128–130). The latter study also indicated that oligosaccharides of 4 or higher degrees of polymerization (i.e., maltotetraose) were detected by a STR-independent lingual taste pathway in humans.…”

Acceptability of flavoured pharmaceutically non-active mini-tablets in pet cats tested with a rapid 3-portal acceptance test with and without food

“…However, it was not found to be palatable in our trial. On the other hand, it is detected through T1R2 and T1R3 sweet taste receptors ( Pullicin, Penner, & Lim, 2017 ), and cats genetically lack the functional T1R2 receptor ( Li et al., 2005 ).…”