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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 ?-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.

SUBMITTER: Pullicin AJ

PROVIDER: S-EPMC5574539 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Human taste detection of glucose oligomers with low degree of polymerization.

Pullicin Alexa J AJ Penner Michael H MH Lim Juyun J

PloS one 20170829 8

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 ...[more]

PMID: 28850567

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Project description:The taste stimulus glucose comprises approximately half of the commercial sugar sweeteners used today, whether in the form of the di-saccharide sucrose (glucose-fructose) or half of high-fructose corn syrup (HFCS). Therefore, oral glucose has been presumed to contribute to the sweet taste of foods when combined with fructose. In light of recent rodent data on the role of oral metabolic glucose signaling, we examined psychopharmacologically whether oral glucose detection may also involve an additional pathway in humans to the traditional sweet taste transduction via the class 1 taste receptors T1R2/T1R3. In a series of experiments, we first compared oral glucose detection thresholds to sucralose thresholds without and with addition of the T1R receptor inhibitor Na-lactisole. Next, we compared oral detection thresholds of glucose to sucralose and to the non-metabolizable glucose analog, α-methyl-D-glucopyranoside (MDG) without and with the addition of the glucose co-transport component sodium (NaCl). Finally, we compared oral detection thresholds for glucose, MDG, fructose, and sucralose without and with the sodium-glucose co-transporter (SGLT) inhibitor phlorizin. In each experiment, psychopharmacological data were consistent with glucose engaging an additional signaling pathway to the sweet taste receptor T1R2/T1R3 pathway. Na-lactisole addition impaired detection of the non-caloric sweetener sucralose much more than it did glucose, consistent with glucose using an additional signaling pathway. The addition of NaCl had a beneficial impact on the detection of glucose and its analog MDG and impaired sucralose detection, consistent with glucose utilizing a sodium-glucose co-transporter. The addition of the SGLT inhibitor phlorizin impaired detection of glucose and MDG more than it did sucralose, and had no effect on fructose, further evidence consistent with glucose utilizing a sodium-glucose co-transporter. Together, these results support the idea that oral detection of glucose engages two signaling pathways: one that is comprised of the T1R2/T1R3 sweet taste receptor and the other that utilizes an SGLT glucose transporter.

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Human taste detection of glucose oligomers with low degree of polymerization.

Publications

Human taste detection of glucose oligomers with low degree of polymerization.

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