Sweet Taste

Sweet taste is a sensation produced on the tongue by molecules that bind to sweet taste receptors, whose structure and genetic origin have recently been uncovered. The sensation of sweetness begins with the transduction by receptors throughout the tongue, or in whatever receptor organ these receptors are present for lower organisms, of the taste signal from a solution containing sweet-tasting molecules. The receptors are heterodimers of two G protein coupled receptors, T1R2 and T1R3, which are expressed by genes at the Sac locus on mouse chromosome 4 and the corresponding Tas1r3 locus in humans.

Taste transduction is the process by which a neural signal is generated following the binding of the tasted molecule to the receptor proteins. It involves a series of chemical reactions that change the resting membrane potential on neurons that produce action potentials carried along the seventh and ninth cranial nerves. These nerves synapse in the brain stem at the parabrachial nucleus where inputs from other visceral organs are combined and then relayed to the thalamus, hypothalamus, and cortex of the brain. Processing at each of these levels results in the ability to perceive taste quality, intensity, and affect (the positive or negative acceptance or rejection magnitude).

It has long been proposed that sweet taste leads to overconsumption of energy and, consequently, obesity.

Sweet solutions that occur in foods and beverages have both positive and negative acceptance/rejection reactions depending upon the individual, state of health or disease, previous consumption, and learned associations with the consequences of the consuming the taste. Generally, humans prefer concentrations of sucrose at approximately 10 percent (weight/volume). Lower and higher concentrations are rejected in comparison to the preferred level, which is also the level at which ratings of liking are highest. In rats, used frequently as animal models for obesity, however, increases in sweetness (independent of postingestional signals) lead to increased responding to obtain it.

The affective reactions to sweet taste are mediated by several neurotransmitters released into various regions of the brain, including the striatum and nucleus accombens. Both dopamine and opioid neurotransmitters appear to be involved in the mediation of the positive rewarding effects of sweet taste. Because sweet tastes are frequently present as sugars in energy-containing foods and beverages, it has long been proposed that sweet taste leads to overconsumption of energy and, consequently, obesity.

However, careful examination of the evidence is not definitive. Although sugar accounts for 22 percent of the American diet, obese individuals have been reported to prefer lower levels of sweetness than nonobese individuals by some investigators, but higher levels by others. Scaling of the level of liking may have led to these differences and more definitive work is needed. On the other hand, recent study demonstrated that in a group that included obese Pima Indians subjects who had a higher preference for sweet tasting food also had higher rates of weight gain after a 2-year follow-up.

Despite the lack of strong evidence, artificial sweeteners will probably continue to be used by many people who wish to limit energy consumption. Provided the energy spared by substituting nonenergy-containing sweeteners for sugars in foods and beverages is not made [Page 734]up from other foods, this could be an effective strategy. However, there is little doubt that sweet-tasting foods of equivalent nutritional content will be chosen more often and eaten in larger quantities than nonsweet tasting foods. Therefore, an even better strategy would be for people to learn to consume less sweet foods. Sweet tastes also can induce metabolic changes by means of cephalic phase insulin release, which could potentially contribute to overconsumption or excessive fat deposition.

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