Emerging Science on Sugar Reduction and Sweetness Perception

Sweet and Umami Taste Receptors-Monell source

T1R2 and T1R3 taste receptors are the primary detectors for sweet taste. Both control and knockout mice (lacking the T1R3 receptor) can detect caloric sweeteners, but mice without T1R3 receptors do not respond to artificial sweeteners.

Posted May 5, 2018—

The 2nd Annual Sweetener Systems Conference was held November 7, 2017. This website is an excerpt from the 2017 Sweetener Systems Conference magazine (post-conference summary).

“Humans have a strong preference for sweet taste, but that’s a problem from a health perspective. In order to develop reduced-sugar products, food formulators need to understand how sweet taste works,” said Nancy E. Rawson, Ph.D., Associate Director of the Monell Chemical Senses Center, Philadelphia. Completely eliminating caloric sugars from reduced-sugar products makes no sense, a concept that led to the title of her presentation: “Why No Calorie Makes No Sense.”

Reducing sugar content is a priority, especially when developing products for children. Food formulators already have a large tool box, including non-nutritive sweeteners, high-potency sweeteners, sugar alternatives, polyols, sensory interactions and physical approaches. But this is not enough.

About 20 years ago, the taste receptors for sweet and umami were discovered. According to Rawson, these T1R genes are believed to have evolved from species that lived more than 400 million years ago. Evolution matches sensory apparatus to nutrition requirements, and each species must solve the fundamental problem of obtaining sufficient nutrients while avoiding being poisoned. Sugars provide a rapidly accessed source of calories necessary for omnivore survival. By replacing caloric sweeteners with non-caloric ones, we are trying to fool Mother Nature. But this is not working, because the brain response to non-caloric sweeteners is different than the response to caloric sweeteners.

To understand sweet taste, one needs to understand taste detectors. The tongue’s taste cells are the initial chemosensors of the alimentary tract. The tongue contains papillae, and taste buds line the mucus-filled cavities of these papillae. In order for a food to be perceived as sweet, a compound has to get to the cells in these crevices.

Rawson explained that there are three types of taste cells within each taste bud. Type I taste cells are probably involved in tasting salt and managing ionic concentration. Type II cells are responsi-ble for detecting sweet, umami and bitter tastes. When activated, Type II cells release ATP, which communicates with type III cells and nerves.

T1R2 and T1R3 taste receptors are the primary detectors for sweet taste. Both control mice and knockout mice (lacking the T1R3 receptor) respond to caloric sweeteners, but the response to artificial sweeteners is eliminated in knockout mice. An independent sugar-detection pathway is made up of glucose transporters. These transporters take up glucose, which is metabolized to generate ATP, leading to downstream signalling and sweet detection. (See chart “Taste Receptors for Sweet and Umami Perception.”)

There are also brush border digestive enzymes (BBE) located in the taste buds. These BBE and amylases are present in sufficient quantity to break down starches and disaccharides into glucose and fructose. This enzymatic pathway is sufficiently active to con-tribute to sweet detection. If you eliminate both the T1R3 and enzyme pathways, you abolish the response to disaccharides.

The second sweet-detection pathway is sensitive only to sugars that can be transported by glucose transporters, i.e., monosaccharides. Non-nutritive sweeteners only act on the first pathway. Nutritive sweeteners act on both pathways, although these are not equal. Thus, taste cells are providing information on both perceptual and nutritional quality. A new definition of sweet will need to encompass the ability of taste cells to detect caloric content.

Is it possible to shift preference for sweet foods? Paul Wise and colleagues reduced dietary sugar intake of subjects by 40% vs. a control group. After four months, subjects in the low-sugar group perceived a pudding as sweeter. But this effect did not persist. One month after discontinuing the reduced-sugar diet, the subjects went back to baseline.

Shifting preference for sweet is going to be harder than shifting preference for salt. Some people have a lot of alpha amylase enzyme, while others don’t have as much. This variation alters the sensory response to polysaccharides. Genetic variation accounts for 23-30% of the total phenotypic variation in perceived intensity across a set of sweeteners, which influences, but does not fully account for, differences in our sweet-taste experience.

Humans have an inborn drive for sources of energy, driven by 400 million years of evolution. So, we are not going to fool Mother Nature very easily. The true target for a sweetener needs to include a caloric component. Companies should strive for sugar reduction, not elimination.

“Why No Calorie Makes No Sense,” Nancy E. Rawson, Ph.D., Associate Director of the Monell Chemical Senses Center,  nrawson@monell.org


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