The motivation to live a healthier life by reducing sugar intake in commercial foods dates back to the late 1800's. Ira Remsen and Constantin Fahlberg published the discovery of saccharin in 1879. Shortly thereafter Fahlberg sold saccharin for use in beverages as a dietetic aid. Although it remains highly desirable to reduce sugar calories in one's diet, we understand today (almost 140 years later) that ingested sugar does more than simply elicit sweet taste. Foremost, sugar elicits a reward signal that triggers liking and motivates repeat consumption. The basis for this reward is the subject of ongoing studies, but, according to mouse studies, sugar also acts upon an oral calorie-detecting pathway that is distinct from the canonical T1r2-T1r3 "sweet taste" receptor.  We also know now that T1r2-T1r3 is expressed not only in the mouth but throughout the gastro-intestinal tract, where it stimulates metabolic incretin hormone responses and modulates sugar uptake into the body via sugar transporters. Furthermore, the same "sweet-taste" receptor has been found in all major metabolic tissues and organs including the pancreas, liver, brain, and adipose tissue. I will discuss the implications of replacing sugars with sweet taste enhancers and substitutes.

When we modulate sweet taste, what else are we modulating?

256th National Meeting (2018)

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