Researchers discover how we perceive bitter taste

Humans can sense five different tastes: sour, sweet, umami, bitter, and salty, using specialized sensors on our tongues called taste receptors. Other than allowing us to enjoy delicious foods, the sensation of taste allows us to determine the chemical makeup of food and prevents us from consuming toxic substances.

Researchers at the UNC School of Medicine, including Bryan Roth, MD, PhD, the Michael Hooker Distinguished Professor of Pharmacology, and Yoojoong Kim, PhD, a postdoctoral researcher in the Roth Lab, recently set out to address one very basic question: "How exactly do we perceive bitter taste?"

A new study, published in Nature, reveals the detailed protein structure of the TAS2R14 bitter taste receptor. In addition to solving the structure of this taste receptor, the researchers were also able to determine where bitter-tasting substances bind to TAS2R14 and how they activate them, allowing us to taste bitter substances.

"Scientists know very little about the structural make up of sweet, bitter, and umami taste receptors," said Kim. "Using a combination of biochemical and computational methods, we now know the structure of the bitter taste receptor TAS2R14 and the mechanisms that initializes the sensation of bitter taste in our tongues."

This detailed information is important for discovering and designing drug candidates that can directly regulate taste receptors, with the potential to treat metabolic diseases such as obesity and diabetes.

From Chemicals to Electricity to Sensation

TAS2R14s are members of the G protein-coupled receptor (GPCR) family of bitter taste receptors. The receptors are attached to a protein known as a G protein. TAS2R14 stands out from the others in its family because it can identify more than 100 distinct substances known as bitter tastants.

Researchers found that when bitter tastants come into contact with TAS2R14 receptors, the chemicals wedge themselves into to a specific spot on the receptor called an allosteric site, this causes the protein to change its shape, activating the attached G protein.

This triggers a series of biochemical reactions within the taste receptor cell, leading to activation of the receptor, which can then send signals to tiny nerve fibers -- through the cranial nerves in the face -- to an area of the brain called the gustatory cortex. It is here where the brain processes and perceives the signals as bitterness. And of course, this complex signaling system occurs almost instantaneously.

Cholesterol's Role in Bitter Taste Reception

While working to define its structure, researchers found another unique feature of TAS2R14 -- that cholesterol is giving it a helping hand in its activation.

"Cholesterol was residing in another binding site called the orthosteric pocket in TAS2R14, while the bitter tastant binds to the allosteric site," said Kim. "Through molecular dynamics simulations, we also found that the cholesterol puts the receptor in a semi-active state, so it can be easily activated by the bitter tastant."

Bile acids, which are created in the liver, have similar chemical structures with cholesterol. Previous studies have suggested that bile acids can bind and activate TAS2R14, but little is known about how and where they bind in the receptor.

Using their newfound structure, researchers found that bile acids might be binding to the same orthosteric pocket as cholesterol. While the exact role of bile acid or cholesterol in TAS2R14 remains unknown, it may play a role in the metabolism of these substances or in relation to metabolic disorders such as obesity or diabetes.

How This Can Help Drug Development

The discovery of this novel allosteric binding site for bitter tasting substances is unique.

The allosteric binding region is located between TAS2R14 and its coupled G protein is called G-protein alpha. This region is critical to form a signaling complex, which helps to transfer the signal from the taste receptor to the G-protein to the taste receptor cells.

"In the future, this structure will be key to discovering and designing drug candidates that can directly regulate G proteins through the allosteric sites," said Kim. "We also have the ability to affect specific G-protein subtypes, like G-protein alpha or G-protein beta, rather than other G-protein pathways that we don't want to cause any other side effects."

Roth and Kim have made a number of new discoveries, but some leave more questions than answers. While running a genomics study, they found that the TAS2R14 protein in complex with the GI is expressed outside the tongue, especially in the cerebellum in the brain, the thyroid, and the pancreas. Researchers are planning future studies to elucidate the function these proteins may have outside of the mouth.

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From the first bite, our sense of taste helps pace our eating

When you eagerly dig into a long-awaited dinner, signals from your stomach to your brain keep you from eating so much you'll regret it -- or so it's been thought. That theory had never really been directly tested until a team of scientists at UC San Francisco recently took up the question.

The picture, it turns out, is a little different.

The team, led by Zachary Knight, PhD, a UCSF professor of physiology in the Kavli Institute for Fundamental Neuroscience, discovered that it's our sense of taste that pulls us back from the brink of food inhalation on a hungry day. Stimulated by the perception of flavor, a set of neurons -- a type of brain cell -- leaps to attention almost immediately to curtail our food intake.

"We've uncovered a logic the brainstem uses to control how fast and how much we eat, using two different kinds of signals, one coming from the mouth, and one coming much later from the gut," said Knight, who is also an investigator with the Howard Hughes Medical Institute and a member of the UCSF Weill Institute for Neurosciences. "This discovery gives us a new framework to understand how we control our eating."

The study, which appears Nov. 22, 2023 in Nature, could help reveal exactly how weight-loss drugs like Ozempic work, and how to make them more effective.

New views into the brainstem

Pavlov proposed over a century ago that the sight, smell and taste of food are important for regulating digestion. More recent studies in the 1970s and 1980s have also suggested that the taste of food may restrain how fast we eat, but it's been impossible to study the relevant brain activity during eating because the brain cells that control this process are located deep in the brainstem, making them hard to access or record in an animal that's awake.

Over the years, the idea had been forgotten, Knight said.

New techniques developed by lead author Truong Ly, PhD, a graduate student in Knight's lab, allowed for the first-ever imaging and recording of a brainstem structure critical for feeling full, called the nucleus of the solitary tract, or NTS, in an awake, active mouse. He used those techniques to look at two types of neurons that have been known for decades to have a role in food intake.

The team found that when they put food directly into the mouse's stomach, brain cells called PRLH (for prolactin-releasing hormone) were activated by nutrient signals sent from the GI tract, in line with traditional thinking and the results of prior studies.

However, when they allowed the mice to eat the food as they normally would, those signals from the gut didn't show up. Instead, the PRLH brain cells switched to a new activity pattern that was entirely controlled by signals from the mouth.

"It was a total surprise that these cells were activated by the perception of taste," said Ly. "It shows that there are other components of the appetite-control system that we should be thinking about."

While it may seem counterintuitive for our brains to slow eating when we're hungry, the brain is actually using the taste of food in two different ways at the same time. One part is saying, "This tastes good, eat more," and another part is watching how fast you're eating and saying, "Slow down or you're going to be sick."

"The balance between those is how fast you eat," said Knight.

The activity of the PRLH neurons seems to affect how palatable the mice found the food, Ly said. That meshes with our human experience that food is less appetizing once you've had your fill of it.

Brain cells that inspire weight-loss drugs

The PRLH-neuron-induced slowdown also makes sense in terms of timing. The taste of food triggers these neurons to switch their activity in seconds, from keeping tabs on the gut to responding to signals from the mouth.

Meanwhile, it takes many minutes for a different group of brain cells, called CGC neurons, to begin responding to signals from the stomach and intestines. These cells act over much slower time scales -- tens of minutes -- and can hold back hunger for a much longer period of time.

"Together, these two sets of neurons create a feed-forward, feed-back loop," said Knight. "One is using taste to slow things down and anticipate what's coming. The other is using a gut signal to say, 'This is how much I really ate. Ok, I'm full now!'"

The CGC brain cells' response to stretch signals from the gut is to release GLP-1, the hormone mimicked by Ozempic, Wegovy and other new weight-loss drugs.

These drugs act on the same region of the brainstem that Ly's technology has finally allowed researchers to study. "Now we have a way of teasing apart what's happening in the brain that makes these drugs work," he said.

A deeper understanding of how signals from different parts of the body control appetite would open doors to designing weight-loss regimens designed for the individual ways people eat by optimizing how the signals from the two sets of brain cells interact, the researchers said.

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Evolution of taste: Early sharks were able to perceive bitter substances

A research team from the University of Cologne, in collaboration with colleagues from the Leibniz Institute for Food Systems Biology in Freising, has discovered a receptor for bitter taste in twelve different cartilaginous fish (sharks and rays). The receptor belongs to the so-called taste receptors type 2 (T2R), which also make humans perceive bitter and potentially toxic foods. Until now, it was assumed that such receptors only occur in bony vertebrates. The work was published under the title 'A singular shark bitter taste receptor provides insights into the evolution of bitter taste perception' in the journal Proceedings of the National Academy of Sciences (PNAS).

In the past, molecular research has had limited information on sharks, as their genomes are often relatively large. Therefore, sequencing is often more complex and takes longer than with many other animals. However, the techniques are more advanced nowadays, providing ever more information on the gene sequences of many cartilaginous fishes. This enabled the neurobiologists lecturer (Privatdozent) Dr Maik Behrens and Tatjana Lang from the Leibniz Institute for Food Systems Biology and Professor Dr Sigrun Korsching at the Institute of Genetics of the University of Cologne to specifically search for bitter taste receptors in cartilaginous fish.

Twelve out of seventeen cartilaginous fish genomes studied contained genes for the taste receptors type 2, with only one T2R gene present in each species. The researchers named this single gene T2R1. The fact that only a single T2R gene was found suggests that it is the original form of these bitter taste receptors, which was not altered by gene duplication and subsequent different specialization of the resulting receptors.

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And then there were 6 -- kinds of taste, that is

Japanese scientist Kikunae Ikeda first proposed umami as a basic taste -- in addition to sweet, sour, salty and bitter -- in the early 1900s. About eight decades later, the scientific community officially agreed with him.

Now, scientists led by researchers at the USC Dornsife College of Letters, Arts and Sciences have evidence of a sixth basic taste.

In research published Oct. 10 in Nature Communications, USC Dornsife neuroscientist Emily Liman and her team found that the tongue responds to ammonium chloride through the same protein receptor that signals sour taste.

"If you live in a Scandinavian country, you will be familiar with and may like this taste," says Liman, professor of biological sciences. In some northern European countries, salt licorice has been a popular candy at least since the early 20th century. The treat counts among its ingredients salmiak salt, or ammonium chloride.

Scientists have for decades recognized that the tongue responds strongly to ammonium chloride. However, despite extensive research, the specific tongue receptors that react to it remained elusive.

Liman and the research team thought they might have an answer.

In recent years, they uncovered the protein responsible for detecting sour taste. That protein, called OTOP1, sits within cell membranes and forms a channel for hydrogen ions moving into the cell.

Hydrogen ions are the key component of acids, and as foodies everywhere know, the tongue senses acid as sour. That's why lemonade (rich in citric and ascorbic acids), vinegar (acetic acid) and other acidic foods impart a zing of tartness when they hit the tongue. Hydrogen ions from these acidic substances move into taste receptor cells through the OTOP1 channel.

Because ammonium chloride can affect the concentration of acid -- that is, hydrogen ions -- within a cell, the team wondered if it could somehow trigger OTOP1.

To answer this question, they introduced the Otop1 gene into lab-grown human cells so the cells produce the OTOP1 receptor protein. They then exposed the cells to acid or to ammonium chloride and measured the responses.

"We saw that ammonium chloride is a really strong activator of the OTOP1 channel," Liman said. "It activates as well or better than acids."

Ammonium chloride gives off small amounts of ammonia, which moves inside the cell and raises the pH, making it more alkaline, which means fewer hydrogen ions.

"This pH difference drives a proton influx through the OTOP1 channel," explained Ziyu Liang, a PhD student in Liman's lab and first author on the study.

To confirm that their result was more than a laboratory artifact, they turned to a technique that measures electrical conductivity, simulating how nerves conduct a signal. Using taste bud cells from normal mice and from mice the lab previously genetically engineered to not produce OTOP1, they measured how well the taste cells generated electrical responses called action potentials when ammonium chloride is introduced.

Taste bud cells from wildtype mice showed a sharp increase in action potentials after ammonium chloride was added while taste bud cells from the mice lacking OTOP1 failed to respond to the salt. This confirmed their hypothesis that OTOP1 responds to the salt, generating an electrical signal in taste bud cells.

The same was true when another member of the research team, Courtney Wilson, recorded signals from the nerves that innervate the taste cells. She saw the nerves respond to addition of ammonium chloride in normal mice but not in mice lacking OTOP1.

Then the team went one step further and examined how mice react when given a choice to drink either plain water or water laced with ammonium chloride. For these experiments, they disabled the bitter cells that also contribute to the taste of ammonium chloride. Mice with a functional OTOP1 protein found the taste of ammonium chloride unappealing and did not drink the solution, while mice lacking the OTOP1 protein did not mind the alkaline salt, even at very high concentrations.

"This was really the clincher," Liman said. "It shows that the OTOP1 channel is essential for the behavioral response to ammonium."

But the scientists weren't done. They wondered if other animals would also be sensitive to and use their OTOP1 channels to detect ammonium. They found that the OTOP1 channel in some species seems to be more sensitive to ammonium chloride than in other species. And human OTOP1 channels were also sensitive to ammonium chloride.

So, what is the advantage in tasting ammonium chloride and why is it evolutionarily so conserved?

Liman speculates that the ability to taste ammonium chloride might have evolved to help organisms avoid eating harmful biological substances that have high concentrations of ammonium.

"Ammonium is found in waste products -- think of fertilizer -- and is somewhat toxic," she explained, "so it makes sense we evolved taste mechanisms to detect it. Chicken OTOP1 is much more sensitive to ammonium than zebra fish." Liman speculates that these variations may reflect differences in the ecological niches of different animals. "Fish may simply not encounter much ammonium in the water, while chicken coops are filled with ammonium that needs to be avoided and not eaten."

But she cautions that this is very early research and further study is needed to understand species differences in sensitivity to ammonium and what makes OTOP1 channels from some species sensitive and some less sensitive to ammonium.

Towards this end, they have made a start. "We identified a particular part of the OTOP1 channel -- a specific amino acid -- that's necessary for it to respond to ammonium," Liman said. "If we mutate this one residue, the channel is not nearly as sensitive to ammonium, but it still responds to acid."

Moreover, because this one amino acid is conserved across different species, there must have been selective pressure to maintain it, she says. In other words, the OTOP1 channel's ability to respond to ammonium must have been important to the animals' survival.

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New role for taste receptors

Taste receptors for bitter substances are not only found on the tongue but also on cells outside the oral cavity. As a new study by the Leibniz Institute for Food Systems Biology at the Technical University of Munich now shows, extraoral bitter taste receptors could also serve as endogenous sensors for bile acids. This discovery suggests that, in addition to food components, endogenous substances may have influenced the evolution of bitter taste receptors. Furthermore, the study provides new approaches to explore the health effects of food constituents in which extraoral bitter taste receptors are involved.

As taste sensors, bitter taste receptors serve to detect and avoid potential toxins in food. Relatively recent findings also indicate that bitter taste receptors are also found on cells of the lung, brain, and gastrointestinal tract, and on blood and sperm cells. A fact that suggests further, less well-studied receptor functions in the body, especially since the human body also produces bitter substances itself.

Based on these findings, the question arises whether bitter taste receptors evolved primarily as taste receptors or rather as endogenous sensors interacting with endogenous bitter substances. The latter, of course, would require that concentrations of endogenous substances in the corresponding body fluids be sufficient to activate endogenous bitter taste receptors on extraoral tissues and cells.

Bile acids are endogenous bitter substances

Bile acids are a good example of endogenous bitter substances and are present in various body fluids. Therefore, a team led by Maik Behrens from the Leibniz Institute in Freising, Germany, investigated which of the approximately 25 human bitter taste receptor types respond to physiologically relevant bile acid concentrations. For this purpose, the team used an established cellular test system and combined functional experiments with molecular modeling approaches. The eight bile acids tested included primary, secondary, tertiary, and conjugated bile acids.

As the team shows, five bitter taste receptor types respond to the bile acids tested. "In this context, the measured activation thresholds of the receptors matched very well the bile acid concentrations reported for human body fluids in the literature," says Florian Ziegler, a doctoral student at the Leibniz Institute who contributed significantly to the study. "Moreover, we were not only able to characterize the binding of bile acids to the bitter taste receptor TAS2R1 by modeling studies but even reproduced the differences of experimental activity data," adds Antonella Di Pizio, who heads the Molecular Modeling group at the Leibniz Institute.

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How tasty is the food?

To know when it's time for a meal -- and when to stop eating again -- is important to survive and to stay healthy, for humans and animals alike. Researchers at the Max Planck Institute for Biological Intelligence investigated how the brain regulates feeding behavior in mice. The team found that the hormone ghrelin activates specialized nerve cells in a brain region known as the amygdala. Here, the interaction between ghrelin and the specialized neurons promotes food consumption and conveys hunger and the pleasant and rewarding feelings associated with eating.

Hunger is a powerful sensation with important biological underpinnings. It signals the body to look for food, which is a crucial behavior to prevent starvation and ensure survival. When we're hungry, we crave for food -- and when we finally get to eat, our body rewards us with pleasant feelings and a general state of happiness.

A network of brain circuits and signaling pathways orchestrates the eating behavior of humans and animals and elicits the associated sensations. One of the central players in this network is the hormone ghrelin. It is released by stomach cells when humans and animals are hungry or fasting, and promotes feeding behavior.

The department of Rüdiger Klein at the Max Planck Institute for Biological Intelligence studies the brain networks that underly feeding behavior in mice. To this end, the researchers conducted a thorough analysis of the different cell types in a brain region known as the central amygdala. "Previously, the amygdala had mostly been studied in the context of feelings like fear and reward, while the regulation of feeding was thought to happen in different parts of the brain, such as the hypothalamus," says Christian Peters, a postdoctoral researcher in the department.

Nine cell clusters

Peters and his colleagues analyzed individual cells in the central amygdala, studying messenger RNA molecules -- the cell's working copies of their genes. The analysis revealed that the cells are organized into nine different cell clusters. Some of these clusters promote appetite while others inhibit it, and they adjust their production of messenger RNAs when the mice are fed or fasting.

"We now have a much better understanding of the diversity of cell types and the physiological processes that promote feeding in the central amygdala," says Rüdiger Klein. "Our research uncovers for the first time that the 'hunger hormone' ghrelin also acts on cells in the central amygdala." There, it activates a small subset of cell clusters, collectively marked by the presence of the protein Htr2a, to increase feeding.

Multiple functions for ghrelin

The scientists found that the Htr2a neurons became active after an overnight fast or when stimulated by the hormone ghrelin. The cells also responded when the researchers presented food to the mice. "We think that ghrelin performs multiple functions," explains Christian Peters. "When mice are hungry, ghrelin activates the appetitive brain regions to predispose the animals for eating. In addition, the hormone enhances the activity in brain circuits, such as the amygdala, that confer rewards, which is likely an incentive to eat additional food." This way, ghrelin increases the palatability of food in proportion to how satiated the mice currently are.

After a fasting diet, when the animals were very hungry the activity of Htr2a neurons was not needed to start feeding, presumably because the tastiness of food is less important under these conditions. "Other brain circuits, for example the hypothalamus, which regulate the body's metabolism, take over and signal the mice that it's important to eat in order to survive," says Christian Peters.

Feeling hungry or satiated has profound impacts on physical but also on emotional wellbeing, as probably everyone knows by the pleasures associated with eating tasty food. "The neuronal networks that convey these feelings are obviously linked to those that control eating, yet it is not fully understood how exactly they influence each other," says Rüdiger Klein.

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How COVID-19 causes neurological damage

It's not uncommon for people to lose their sense of taste and smell due to a Covid-19 infection. In others, the disease has had an even stronger impact on the nervous system, with effects ranging from lasting concentration problems to strokes. Now, researchers led by Professor Gregor Hutter from the Department of Biomedicine at the University of Basel and University Hospital of Basel have reported new insights into the development of "neuro-Covid" in the journal Nature Communications.

Specifically, the team investigated how different severities of neuro-COVID can be detected and predicted by analyzing the cerebrospinal fluid and blood plasma of affected individuals. Their findings also offer some indications of how to prevent neurological damage due to Covid-19.

The study included 40 Covid-19 patients with differing degrees of neurological symptoms. In order to identify typical changes associated with neuro-Covid, the team of researchers compared these individuals' cerebrospinal fluid and blood plasma with samples from a control group. They also measured the brain structures of test subjects and surveyed participants 13 months after their illness in order to identify any lasting symptoms.

Holes in the blood-brain barrier

Particularly in the group with the most serious neurological symptoms, the researchers identified a link with an excessive immune response. On the one hand, affected individuals showed indications of impairment of the blood-brain barrier, which the study's authors speculate was probably triggered by a "cytokine storm" -- a massive release of pro-inflammatory factors in response to the virus.

On the other hand, the researchers also found antibodies that targeted parts of the body's own cells -- in other words, signs of an autoimmune reaction -- as a result of the excessive immune response. "We suspect that these antibodies cross the porous blood-brain barrier into the brain, where they cause damage," explains Hutter. They also identified excessive activation of the immune cells specifically responsible for the brain -- the microglia.

Blood test as a long-term objective

In a further step, Hutter and his team investigated whether the severity of neurological symptoms is also perceptible in brain structures. Indeed, they found that people with serious neuro-Covid symptoms had a lower brain volume than healthy participants at specific locations in the brain and particularly at the olfactory cortex -- that is, the area of the brain responsible for smell.

"We were able to link the signature of certain molecules in the blood and cerebrospinal fluid to an overwhelming immune response in the brain and reduced brain volume in certain areas, as well as neurological symptoms," says Hutter, adding that it is now important to examine these biomarkers in a greater number of participants. The aim would be to develop a blood test that can already predict serious cases, including neuro-Covid and long Covid, at the start of an infection.

Targets for preventing consequential damage

These same biomarkers point to potential targets for drugs aimed at preventing consequential damage due to a Covid-19 infection. One of the biomarkers identified in blood, the factor MCP-3, plays a key role in the excessive immune response, and Hutter believes there is the potential to inhibit this factor medicinally.

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Babies react to taste and smell in the womb

Scientists have recorded the first direct evidence that babies react differently to various smells and tastes while in the womb by looking at their facial expressions.

A study led by Durham University's Fetal and Neonatal Research Lab, UK, took 4D ultrasound scans of 100 pregnant women to see how their unborn babies responded after being exposed to flavours from foods eaten by their mothers.

Researchers looked at how the fetuses reacted to either carrot or kale flavours just a short time after the flavours had been ingested by the mothers.

Fetuses exposed to carrot showed more "laughter-face" responses while those exposed to kale showed more "cry-face" responses.

Their findings could further our understanding of the development of human taste and smell receptors.

The researchers also believe that what pregnant women eat might influence babies' taste preferences after birth and potentially have implications for establishing healthy eating habits.

The study is published in the journal Psychological Science.

Humans experience flavour through a combination of taste and smell. In fetuses it is thought that this might happen through inhaling and swallowing the amniotic fluid in the womb.

Lead researcher Beyza Ustun, a postgraduate researcher in the Fetal and Neonatal Research Lab, Department of Psychology, Durham University, said:

"A number of studies have suggested that babies can taste and smell in the womb, but they are based on post-birth outcomes while our study is the first to see these reactions prior to birth.

"As a result, we think that this repeated exposure to flavours before birth could help to establish food preferences post-birth, which could be important when thinking about messaging around healthy eating and the potential for avoiding 'food-fussiness' when weaning.

"It was really amazing to see unborn babies' reaction to kale or carrot flavours during the scans and share those moments with their parents."

The research team, which also included scientists from Aston University, Birmingham, UK, and the National Centre for Scientific Research-University of Burgundy, France, scanned the mothers, aged 18 to 40, at both 32 weeks and 36 weeks of pregnancy to see fetal facial reactions to the kale and carrot flavours.

Mothers were given a single capsule containing approximately 400mg of carrot or 400mg kale powder around 20 minutes before each scan. They were asked not to consume any food or flavoured drinks one hour before their scans.

The mothers also did not eat or drink anything containing carrot or kale on the day of their scans to control for factors that could affect fetal reactions.

Facial reactions seen in both flavour groups, compared with fetuses in a control group who were not exposed to either flavour, showed that exposure to just a small amount of carrot or kale flavour was enough to stimulate a reaction.

Co-author Professor Nadja Reissland, head of the Fetal and Neonatal Research Lab, Department of Psychology, Durham University, supervised Beyza Ustun's research. She said:

"Previous research conducted in my lab has suggested that 4D ultrasound scans are a way of monitoring fetal reactions to understand how they respond to maternal health behaviours such as smoking, and their mental health including stress, depression, and anxiety.

"This latest study could have important implications for understanding the earliest evidence for fetal abilities to sense and discriminate different flavours and smells from the foods ingested by their mothers."

Co-author Professor Benoist Schaal, of the National Centre for Scientific Research-University of Burgundy, France, said:

"Looking at fetuses' facial reactions we can assume that a range of chemical stimuli pass through maternal diet into the fetal environment.

"This could have important implications for our understanding of the development of our taste and smell receptors, and related perception and memory."

The researchers say their findings might also help with information given to mothers about the importance of taste and healthy diets during pregnancy.

They have now begun a follow-up study with the same babies post-birth to see if the influence of flavours they experienced in the womb affects their acceptance of different foods.

Research co-author Professor Jackie Blissett, of Aston University, said:

"It could be argued that repeated prenatal flavour exposures may lead to preferences for those flavours experienced postnatally. In other words, exposing the fetus to less 'liked' flavours, such as kale, might mean they get used to those flavours in utero.

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Taste, temperature and pain sensations are neurologically linked

If you have eaten a chili pepper, you have likely felt how your body reacts to the spicy hot sensation. New research published by biologists at the University of Oklahoma shows that the brain categorizes taste, temperature and pain-related sensations in a common region of the brain. The researchers suggest the brain also groups these sensations together as either pleasant or aversive, potentially offering new insights into how scientists might better understand the body's response to and treatment of pain.

"The spicy hot sensation you get from a chili pepper is actually a pain sensation…this follows activation of pain-related fibers that innervate the tongue and are heat sensitive," said Christian H. Lemon, Ph.D., an associate professor in the Department of Biology in the Dodge Family College of Arts and Sciences at OU. "What happens is a chemical in chili peppers, called capsaicin, causes activation of pain fibers and 'tricks' the neurons to react like there is a heat stimulus in your mouth, so you'll notice when you eat spicy foods, your body will react to try to remove the heat - your blood vessels can dilate and you can start to sweat because your body 'thinks' it's overheating."

Lemon, who is also a member of the OU Institute for Biomedical Engineering, Science and Technology, and researchers in his lab, Jinrong Li, Ph.D., and?Md Sams Sazzad Ali, Ph.D., published an article in The Journal of Neuroscience that examines how taste, temperature and pain-related sensations interact in the brain. Their article was also selected for the journal's Featured Research section.

"Neural messages associated with pain are partly carried by neural circuits involved with sensing temperature," Lemon said. "This would explain, for example, why when you touch a hot stove, it's a burning pain. There are intimate ties between temperature and pain, and there are intimate ties between temperature and taste…just about everything we eat is either warmed or cooled, and that's known to have a fairly robust effect on the way we perceive certain tastes."

The research team wanted to better understand how temperature and pain intersect with taste neurologically. Building on their previous research that had shown that temperature and taste signals come together in a particular section of the midbrain, Lemon's research group used mouse models under anesthesia to artificially stimulate temperature and pain-related fibers, combined with a physiological method to monitor the actions occurring in the brain to determine the connection between these senses.

"It's been known that temperature and taste can activate some of the same cells in the brain, but this was rarely systematically studied," he said. "We wanted to know if the temperature responses that we were seeing in this part of the brain were actually attributable to activation of thermal and pain-related fibers that innervate the head, face and mouth. To do this we used a modern genetic technology where we could insert a protein into these 'temperature/pain' cells that allowed us to control these cells with blue light -- we could turn the cells on with a light, like a light switch."

"What we found is that these neurons that scientists have studied for a long time as taste neurons actually respond to artificial stimulation of these temperature/pain cells," he added. "This is significant because most scientists that have looked at taste, they're usually only studying neural circuits from the perspective of taste. Pain scientists are usually only looking at pain-related responses, but they actually come together in this part of the midbrain, and not only do they come together, they do so in a very systematic way where preferred tastes and preferred temperatures are separated from adverse taste and temperatures in terms of the way that the responses are happening in this part of the brain."

The researchers categorize preferred or pleasurable tastes as something sweet, like sugar, whereas adverse tastes are bitter -- which can signify that something may be toxic or harmful. Similarly, people, and mice, have preferred temperatures, like a comfortably warmed or cooled environment as compared to an extreme cold or extreme heat stimulus.

Through this artificial stimulation of temperature/pain cells and the corresponding taste neurons, they discovered the brain segregated preferable tastes and temperatures from adverse tastes and temperatures. This finding offers new insights into how these senses interact, which could have implications for how scientists understand the brain's responses to stimuli that cause pain.

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Your gut senses the difference between real sugar and artificial sweetener

Your taste buds may or may not be able to tell real sugar from a sugar substitute, but there are cells in your intestines that can and do distinguish between the two sweet solutions. And they can communicate the difference to your brain in milliseconds.

Not long after the sweet taste receptor was identified in the mouths of mice 20 years ago, scientists attempted to knock those taste buds out. But they were surprised to find that mice could still somehow discern and prefer natural sugar to artificial sweetener, even without a sense of taste.

The answer to this riddle lies much further down in the digestive tract, at the upper end of the gut just after the stomach, according to research led by Diego Bohórquez, an associate professor of medicine and neurobiology in the Duke University School of Medicine.

In a paper appearing Jan. 13 in Nature Neuroscience, "we've identified the cells that make us eat sugar, and they are in the gut," Bohórquez said. Infusing sugar directly into the lower intestine or colon does not have the same effect. The sensing cells are in the upper reaches of the gut, he said.

Having discovered a gut cell called the neuropod cell, Bohórquez with his research team has been pursuing this cell's critical role as a connection between what's inside the gut and its influence in the brain. The gut, he argues, talks directly to the brain, changing our eating behavior. And in the long run, these findings may lead to entirely new ways of treating diseases.

Originally termed enteroendrocrine cells because of their ability to secrete hormones, specialized neuropod cells can communicate with neurons via rapid synaptic connections and are distributed throughout the lining of the upper gut. In addition to producing relatively slow-acting hormone signals, the Bohórquez research team has shown that these cells also produce fast-acting neurotransmitter signals that reach the vagus nerve and then the brain within milliseconds.

Bohórquez said his group's latest findings further show that neuropods are sensory cells of the nervous system just like taste buds in the tongue or the retinal cone cells in the eye that help us see colors.

"These cells work just like the retinal cone cells that that are able to sense the wavelength of light," Bohórquez said. "They sense traces of sugar versus sweetener and then they release different neurotransmitters that go into different cells in the vagus nerve, and ultimately, the animal knows 'this is sugar' or 'this is sweetener.'"

Using lab-grown organoids from mouse and human cells to represent the small intestine and duodenum (upper gut), the researchers showed in a small experiment that real sugar stimulated individual neuropod cells to release glutamate as a neurotransmitter. Artificial sugar triggered the release of a different neurotransmitter, ATP.

Using a technique called optogenetics, the scientists were then able to turn the neuropod cells on and off in the gut of a living mouse to show whether the animal's preference for real sugar was being driven by signals from the gut. The key enabling technology for the optogenetic work was a new flexible waveguide fiber developed by MIT scientists. This flexible fiber delivers light throughout the gut in a living animal to trigger a genetic response that silenced the neuropod cells. With their neuropod cells switched off, the animal no longer showed a clear preference for real sugar.

"We trust our gut with the food we eat," Bohórquez said. "Sugar has both taste and nutritive value and the gut is able to identify both."

"Many people struggle with sugar cravings, and now we have a better understanding of how the gut senses sugars (and why artificial sweeteners don't curb those cravings)," said co-first author Kelly Buchanan, a former Duke University School of Medicine student who is now an Internal Medicine resident at Massachusetts General Hospital. "We hope to target this circuit to treat diseases we see every day in the clinic."

In future work, Bohórquez said he will be showing how these cells also recognize other macronutrients. "We always talk about 'a gut sense,' and say things like 'trust your gut,' well, there's something to this," Bohórquez said.

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COVID-19: Reduced sense of taste and smell lingers

Patients with mild Covid-19 infections experience a significantly increased longer lasting reduced sense of taste and smell. This is also the case for long-term shortness of breath, although relatively few people are affected. And women and the elderly are particularly affected. This is shown by new research findings from Aarhus University Aarhus University Hospital and Regional Hospital West Jutland.

The last 14 months have taught us that there are different symptoms and outcomes of Covid-19. However, the vast majority of people who fall ill with Covid-19 experience mild symptoms and get over the disease in two to three weeks.

These are precisely some of the people who have been the subject of a new study from AUH, HEV and AU. In the study, researchers have compared symptoms on a daily basis for up to 90 days in 210 healthcare workers who had tested positive and 630 with a negative test.

Each day, the participants received a link to a questionnaire on whether they had experienced one of the following symptoms within the last 24 hours: coughing, sore throat, headaches, fever, muscle pain, shortness of breath and reduced sense of taste and smell.

"We saw that the prevalence of a longer lasting reduced taste and smell is significantly increased in patients with mild Covid-19 disease who did not require hospitalisation. This pattern is also seen for shortness of breath, but far fewer people were affected," says Henrik Kolstad, who is behind the study.

Women and the elderly experience more symptoms

Thirty per cent of those who had tested positive and almost none of the participants with a negative test reported a reduced sense of taste and smell over the full ninety days. At the beginning of the project, shortness of breath was reported by twenty per cent of those who had tested positive, with the figure falling to five per cent after thirty days, though without ever reaching the level of the participants who had tested negative.

Coughing, sore throat, headaches, muscle pain and fever were more common among those who tested positive than those who tested negative in the first few days, but after thirty days no increases were seen.

Woman with a positive test reported more symptoms compared to women with a negative test than was the case for men with a positive test when compared to men with a negative test. The same was true for older and younger participants. According to the researcher, this could indicate that women and the elderly are more susceptible to developing long-term COVID-19 symptoms.

"This study provides detailed knowledge of which symptom pathways you can expect after having tested positive for COVID-19 without requiring hospitalisation," says Henrik Kolstad.

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Food protein can eliminate pungency and bitterness of extra virgin olive oil

Researchers have been investigating the potential health-promoting qualities of extra virgin olive oil (EVOO) for decades, including its possible medicinal value for preventing cancer, Alzheimer's, and cardiovascular disease, as part of the well-known Mediterranean diet. However, consumers in the U.S. have been slow to embrace it as a staple in their diet. This reluctance, say scientists, might be in part due to EVOO's bitter taste and pungency, which is caused by the presence of substances known as phenolic compounds, the very ones believed to contribute to EVOO health benefits. In 2005, researchers from the Monell Chemical Senses Center identified one of these compounds as an anti-inflammatory that they named oleocanthal and is mostly responsible for the oil's strong, pungent sensation localized to the throat.

Now, another team from Monell has shown that the presence of certain food proteins, such as those in egg yolk, suppresses EVOO's purported less desirable sensory qualities. The team published their findings in Scientific Reports.

"Knowing that the oil can be consumed without bitterness or stinging sensation might increase the popularity of this healthy food," said first author Catherine Peyrot des Gachons, PhD, a Monell senior research associate. "Our findings show that, in many cases, people are not going to perceive the bitterness and pungency once mixed in food."

While experimenting in the laboratory, investigators put the EVOO into a mayonnaise-like material that would be easier for sensory study participants to assess, rather than drinking unadulterated EVOO from a drinking glass, as is commonly done for EVOO tasting. They discovered that after several hours the oil-mayo mixture was much less pungent and bitter. Even a small amount of egg yolk in the mixture was sufficient to cause this reduction.

"This was a big surprise to us," said coauthor Gary Beauchamp, PhD, Distinguished Member of Monell. "But it probably would not be a surprise to people from the Mediterranean area who are much more familiar with consuming extra virgin olive oil in foods and even neat."

The team showed that proteins in the egg yolk were responsible for eliminating EVOO pungency and bitterness. Others such as whey protein yielded similar sensory suppression. The researchers hypothesize that eliminating bitterness and pungency in EVOO happens when proteins interact with oleocanthal and the bitter-tasting phenolic compounds.

The possibility that oleocanthal could be bound by food protein raises a significant conundrum for scientists. For example, the authors ask, could this binding reduce oleocanthal's medicinal effects in the human body? Or, to the contrary, might it make oleocanthal more available in the human body compared to oleocanthal alone? "We don't know the answer to those questions, but it certainly raises some interesting and important issues of bioavailability of this compound," said Beauchamp.

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Half of young adults with COVID-19 have persistent symptoms 6 months after, study finds

A paper published in the journal Nature Medicine on long-COVID, describes persistent symptoms six months after acute COVID-19, even in young home isolated people.

The study from the Bergen COVID-19 Research Group followed infected patients during the first pandemic wave in Bergen Norway.

"The main novel finding is that more than fifty per cent of young adults up to 30 years old, isolated at home, still have persistent symptoms six months after mild to moderate disease," the leader of the group, Professor Nina Langeland explains.

The most common symptoms were loss of smell and/or taste, fatigue, shortness of breath, impaired concentration, and memory problems.

"There was a significant correlation between high antibody levels and symptoms in home isolated patients, other risk factors for symptoms were asthma or other chronic lung disease," says Professor Rebecca Cox, Head of the Influenza Centre at University of Bergen and Haukeland University Hospital and co-leader of the research group.

Impaired memory and concentration difficulties

In non-hospitalized COVID-19-patients, thirty per cent experienced fatigue which was the most common symptom. Children under the age of 16 years had fewer long-term symptoms than adults, but Associate Professor Bjørn Blomberg, and first author of the article, underlines:

"The cognitive symptoms of impaired memory and concentration difficulties are particularly worrying for young people at school or university and highlights the importance of vaccination to prevent the long-term health implications of COVID-19."

From Science Daily

New study explains why you should look at your food before casting judgment

 The order in which your senses interact with food has a tremendous impact on how much you like it. That's the premise of a new study led by the University of South Florida (USF). The findings published in the Journal of Consumer Psychology show that food tastes better if you see it before smelling it.

Researchers came to this conclusion following four experiments involving cookies, fruit snacks and lemonade. In the first study, nearly 200 participants interacted with the food, each item wrapped in an opaque versus a transparent package. The team administered each item in different orders: visual before scent, scent before visual, only visual and only scent. Despite being the same product, participants rated the strawberry-flavored fruit snacks packaged in an envelope as tasting better when they could see the item before smelling it compared to their counterparts who smelled the item before seeing it. Researchers experienced the same results when they tested taste perception of the cookies.

"This is because being able to see a food item before smelling it helps in processing the scent cue with greater ease, which in turn enhances the food taste perception," said Dipayan Biswas, Frank Harvey Endowed Professor of Marketing at USF. "Basically, scents play a very critical role in influencing taste perceptions; however, interestingly, people can process a scent better in their brains when the scent is preceded by a corresponding visual cue, such as color."

The research team, which includes collaborators from Columbia University and the University of Rhode Island, experienced the same results when it focused on beverages. Researchers poured the same, yellow-colored lemonade into lidded clear plastic cups and lidded solid-colored plastic cups that were splashed with artificial lemon-scented oil. Similarly, participants preferred the drink that they could see before smelling and they drank more of it. Researchers tested consumption by purposely leaving the drinks in front of participants as they undertook an unrelated task. Additionally, the researchers provided the same drinks with the addition of odorless purple food coloring, a color typically not associated with lemon flavor. In this case, it had a negative effect on taste perception, as the color contradicted expectations.

"We tested this to get a better understanding of how the human sensory processing system evaluates a sequence of visual and scent-related cues," Biswas said.

These findings are highly beneficial to supermarkets and Biswas suggests they consider installing more glass cases to help facilitate a customer's ability to see a food item at a distance before smelling it. He suggests strategic displays with photos or samples be visible prior to entering a business, helping strengthen taste perceptions of food items, which can increase sales and overall impression of the business. Biswas emphasizes that the theory also applies to pantry food items, such as potato chips, which may attract more interest if they were sold in transparent packaging.

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What evolution reveals about the function of bitter receptors

 To evaluate the chemical composition of food from a physiological point of view, it is important to know the functions of the receptors that interact with food ingredients. These include receptors for bitter compounds, which first evolved during evolution in bony fishes such as the coelacanth. What 400 million years of evolutionary history reveal about the function of both fish and human bitter receptors was recently published in the journal Genome Biology and Evolution by a team of researchers led by the Leibniz Institute for Food Systems Biology at the Technical University of Munich and the University of Cologne.

Evolutionarily, bitter receptors are a relatively recent invention of nature compared to other chemoreceptors, such as olfactory receptors. Their function of protecting vertebrates from consuming potentially toxic substances has long been scientifically recognized. More recent are observations that bitter receptors have other functions beyond taste perception. These include roles in defense against pathogenic bacteria, in metabolic regulation, and possibly also functions as sensors for endogenous metabolites and hormones.

Coelacanth and zebrafish in comparison

The team of scientists led by biologists Sigrun Korsching of the University of Cologne and Maik Behrens of the Leibniz Institute for Food Systems Biology now provides further evidence to support this hypothesis. In their current study, the team compared two original bitter receptor types from the coelacanth (Latimeria chalumnae) with four others from the zebrafish (Danio rerio) phylogenetically, functionally and structurally. To this end, the research team conducted, among other experiments, extensive functional studies using an established cell-based test system as well as a computer-based modeling approach. The goal was to gain a deep insight into the evolutionary history of bitter receptors in order to learn more about their functions.

As the study results show, both fish species possess, amongst others, a pair of homologous bitter receptor genes that presumably arose from a primordial gene. In this regard, the bitter recognition spectra of these fish receptors were largely identical despite 400 million years of separate evolution, according to the results of the functional studies. "What is particularly exciting about our results is that the original fish receptors recognized substances in the cellular test system which are still detected by human bitter receptors to date. These include bile acids," says co-author Antonella Di Pizio of the Leibniz Institute.

Over 400 million years of selection pressure

"So there must have been selective pressure at least until humans evolved, that means human bitter receptors can still detect the same bitter substances as a bony fish did over 400 million years ago," concludes taste researcher Maik Behrens. Sigrun Korsching adds, "This speaks for one or more important functions of bitter receptors, even during human evolution."

"Coelacanths are carnivores. Therefore, one could speculate that the existence of a bitter receptor variant that mainly recognizes steroid hormones and bile acids protects against the consumption of poisonous fish, which can contain not only bile acids but also highly potent neurotoxins in their liver and gallbladder. For example, the poisonous puffer fish Arothron hispidus lives in the same waters as the coelacanth," says Maik Behrens. "In humans and also in zebrafish, however, it is questionable whether such a receptor variant would have been preserved from an evolutionary point of view if it did not have other functions inside the body. Another argument in favor of such extraoral functions is that bitter receptors are also found on human organs such as the heart, brain or thyroid gland," Behrens added. One goal of his research is to help understand the effects of bitter substances on a systems biological level, regardless of whether they entered the body through food or whether they belong to the body's own substances.

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Sweet taste reduces appetite?

 The sweet taste of sugar is very popular worldwide. In Austria and Germany, the yearly intake per person adds up to about 33 and 34 kilograms, respectively. Thus, sugar plays an increasingly role in the nutrition and health of the population, especially with regard to body weight. However, little is known about the molecular (taste) mechanisms of sugar that influence dietary intake, independently of its caloric load.

Taste receptor and satiety regulation

"We therefore investigated the role of sweet taste receptor activation in the regulation of satiety," says Veronika Somoza, deputy head of the Department of Physiological Chemistry at the University of Vienna and director of the Leibniz Institute for Food Systems Biology at the Technical University of Munich.

For this purpose, the scientists conducted a blinded, cross-over intervention study with glucose and sucrose. A total of 27 healthy, male persons, between 18 and 45 years of age, received either a 10 percent glucose or sucrose solution (weight percent) or one of the sugar solutions supplemented with 60 ppm lactisole. Lactisole is a substance that binds to a subunit of the sweet receptor and reduces the perception of sweet taste. Despite different types of sugar, all solutions with or without lactisole had the same energy content.

Two hours after drinking each of the test solutions, the participants were allowed to have as much as breakfast they wanted. Shortly before and during the 120-min waiting period, the researchers took blood samples in regular intervals and measured their body temperature.

Additional 100 kilocalories on average

After the consumption of the lactisole-containing sucrose solution, the test persons had an increased energy intake from breakfast of about 13 percent, about 100 kilocalories more, than after drinking the sucrose solution without lactisole. In addition, the subjects of this group showed lower body temperature and reduced plasma serotonin concentrations. Serotonin is a neurotransmitter and tissue hormone which, among other things, has an appetite-suppressing effect. In contrast, the researchers observed no differences after administration of the lactisole-containing glucose solution and the pure glucose solution.

"This result suggests that sucrose, regardless of its energy content, modulates the regulation of satiety and energy intake via the sweet taste receptor," says Barbara Lieder, head of Christian Doppler Laboratory for Taste Research and also deputy head of the Department of Physiological Chemistry of the Faculty of Chemistry at University of Vienna.

The first study author of the study, Kerstin Schweiger, University of Vienna adds: "We do not know yet why we could not observe the lactisole effect with glucose. However, we suspect it is because glucose and sucrose activate the sweet receptor in different ways. We also assume that mechanisms independent of the sweet receptor play a role."

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Touch and taste? It's all in the tentacles

 

Suction cups on octopus tentacles

Octopuses have captured the human imagination for centuries, inspiring sagas of sea monsters from Scandinavian kraken legends to TV's "Voyage to the Bottom of the Sea" and, most recently, Netflix's less-threatening "My Octopus Teacher." With their eight suction-cup covered tentacles, their very appearance is unique, and their ability to use those appendages to touch and taste while foraging further sets them apart.

In fact, scientists have wondered for decades how those arms, or more specifically the suction cups on them, do their work, prompting a number of experiments into the biomechanics. But very few have studied what is happening on a molecular level. In a new report, Harvard researchers got a glimpse into how the nervous system in the octopus' arms (which operate largely independently from its centralized brain) manage this feat.

The work published Thursday in Cell.

The scientists identified a novel family of sensors in the first layer of cells inside the suction cups that have adapted to react and detect molecules that don't dissolve well in water. The research suggests these sensors, called chemotactile receptors, use these molecules to help the animal figure out what it's touching and whether that object is prey.

"We think because the molecules do not solubilize well, they could, for instance, be found on the surface of octopuses' prey and [whatever the animals touch]," said Nicholas Bellono, an assistant professor of molecular and cellular biology and the study's senior author. "So, when the octopus touches a rock versus a crab, now its arm knows, 'OK, I'm touching a crab [because] I know there's not only touch but there's also this sort of taste.'"

In addition, scientists found diversity in what the receptors responded to and the signals they then transmitted to the cell and nervous systems.

"We think that this is important because it could facilitate complexity in what the octopus senses and also how it can process a range of signals using its semi-autonomous arm nervous system to produce complex behaviors," Bellono said.

The scientists believe this research can help uncover similar receptor systems in other cephalopods, the invertebrate family that also includes squids and cuttlefish. The hope is to determine how these systems work on a molecular level and answer some relatively unexplored questions about how these creatures' capabilities evolved to suit their environment.

"Not much is known about marine chemotactile behavior and with this receptor family as a model system, we can now study which signals are important for the animal and how they can be encoded," said Lena van Giesen, a postdoctoral fellow in the Bellono Lab and lead author of the paper. "These insights into protein evolution and signal coding go far beyond just cephalopods."

Along with Giesen, other co-authors from the lab include Peter B. Kilian, an animal technician, and Corey A.H. Allard, a postdoctoral fellow.

"The strategies they have evolved in order to solve problems in their environment are unique to them and that inspires a great deal of interest from both scientists and non-scientists alike," Kilian said. "People are drawn to octopuses and other cephalopods because they are wildly different from most other animals."

The team set out to uncover how the receptors are able to sense chemicals and detect signals in what they touch, like a tentacle around a snail, to help them make choices.

Octopus arms are distinct and complex. About two-thirds of an octopus's neurons are located in their arms. Because the arms operate partially independently from the brain, if one is severed it can still reach for, identify, and grasp items.

The team started by identifying which cells in the suckers actually do the detecting. After isolating and cloning the touch and chemical receptors, they inserted them in frog eggs and in human cell lines to study their function in isolation. Nothing like these receptors exists in frog or human cells, so the cells act essentially like closed vessels for the study of these receptors.

The researchers then exposed those cells to molecules such as extracts from octopus prey and others items to which these receptors are known to react. Some test subjects were water-soluble, like salts, sugars, amino acids; others do not dissolve well and are not typically considered of interest by aquatic animals. Surprisingly, only the poorly soluble molecules activated the receptors.

Researchers then went back to the octopuses in their lab to see whether they too responded to those molecules by putting those same extracts on the floors of their tanks. They found the only odorants the octopuses receptors responded to were a non-dissolving class of naturally occurring chemicals known as terpenoid molecules.

"[The octopus] was highly responsive to only the part of the floor that had the molecule infused," Bellono said. This led the researchers to believe that the receptors they identified pick up on these types of molecules and help the octopus distinguish what it's touching. "With the semi-autonomous nervous system, it can quickly make this decision: 'Do I contract and grab this crab or keep searching?'"

While the study provides a molecular explanation for this aquatic touch-taste sensation in octopuses through their chemotactile receptors, the researchers suggest further study is needed, given that a great number of unknown natural compounds could also stimulate these receptors to mediate complex behaviors.

"We're now trying to look at other natural molecules that these animals might detect," Bellono said.

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