Why do we love sweet taste?
Date: June 01, 2006
Title: “Why do we love sweets? Roles of ‘Taste’ Receptors Beyond the Tongue”
Speaker’s Name and Affiliation: Dr. Anthony Sclafani (in place of the scheduled speaker, Dr. Michael Lewis), Brooklyn College
The originally scheduled speaker, Dr. Michael Lewis, had to cancel his talk due to circumstances beyond his control. Fortunately, Dr. Sclafani from Brooklyn College had a talk prepared for the American Diabetes Association meeting, and he was able to give this talk in place of the originally scheduled seminar.
Dr. Sclafani spoke on the role of sweet taste receptors beyond those found on the tongue in the determination of sweet preferences in animals. The discovery of the sweet taste receptor in 2000 was a major and important discovery for researchers who study sweet taste preferences. This shed light on the molecular basis of sweet taste, and improved our understanding of this complicated and fascinating system. Since this time, sweet taste receptors have been located on a variety of tissues, but the role they play in flavor learning is unclear.
Dr. Sclafani has spent his career studying sweet taste in animals to determine how and why sweet preferences are acquired. One of the most powerful experimental models used to decipher this is the sham-feeding model, where a gastric fistula is inserted into the stomach of the animal so that everything that is ingested drains out before it is absorbed. With this type of model, one can differentiate the effects of sweet taste from post-ingestive effects of the nutrient. When you compare intake of sugar/sweet solutions in animals that have previously had experience with sucrose, sham-fed animals will have higher intakes than control animals. This likely occurs because animals are not experiencing the post-ingestive effects of the nutrient, so they continue to consume in absence of the appropriate feedback signals from the gut.
In addition to the fact that sweet taste receptors on the tongue influence intake directly, there are also “nutrient reward” signals that act directly upon the gut to control food intake. Glucose can be infused directly into the gut while the animal consumes flavored Kool-Aid, and the animal will show a preference for the flavors that are paired with glucose infusions, regardless of what the flavor is. Both gastric and duodenal infusions of glucose result in increased intake, while hepatic infusions show no difference in intake between glucose and water infusions. Taste receptor cells that have been found in the gut might play a role in this “nutrient reward” learning.
Currently, it is not known how sweet taste and post-oral feedback signals act on the brain to influence taste preferences. They likely affect both the reward and feeding systems. With continually improving technologies to identify the pertinent genes and signals involved in these processes, future advancements in this field are likely.
Q. Do animals have to be trained before you open the fistula, or when you open the fistula for the first time, do they increase their intake?
A. Experience is important, but animals will increase their intake the first time you open the fistula by about 50%. The concentration of sucrose in the stimulus is also important.
Q. If you had animals trained on 10% sucrose, would you still get this sham feeding effect?
A. No one has reported a reduction in intake in sham-fed animals, after the fistula is removed. I have once, but only when animals are first conditioned with saccharin.
Q. Could you comment on fructose? I understand that it doesn’t result in insulin release, but are animals satiated after consuming it?
A. In animals, fructose is just as satiating as other sugars. But, the findings in humans are not as clear.
Q. Is this interval long enough to cause extinction?
A. We’ve given animals as long as 40 days and they still don’t show a decrease in their preferences for the flavors paired with nutrients.
Q. In your earlier slides, you showed that gastric effects of nutrients produce satiation. Is it possible that the sensations they produce are actually reward sensations?
A. We believe that reward signals are different from satiation signals.
Q. Is the rate of infusion of glucose (duodenal and hepatic) one of the variables that affects intake?
A. We have debated that, and I’m not sure what the best infusion rate is. We use 2 hour infusion rates.
Q. Have you ever infused further down in the intestine?
A. We’ve thought about infusions in the ileum, but haven’t done that as of yet. It’s a good point.
Q. What is the role of gustducin? Can you block the action of gustducin?
A. Gustducin is the second messenger involved in perception of bitter and sweet taste. You can, in effect, block the action of gustducin by knocking our the gustducin gene.
Q. Wouldn’t the stimulus from the intestine be controlled by the vagus?
A. Vagotomy does not interfere with nutrient learning, so this is not really a factor.
Q. Do you interpret the different responses between saccharin and sucrose to “nutrient reward?”
Q. If the animal tastes the sucrose and saccharin and doesn’t swallow it, what happens?
A. If we sham-feed the animals with these nutrients, it will drive intake once the fistula is opened.
Q. Does sucralose have a GI effect that is similar to that of other sugar alcohols?
A. Not to my knowledge.