The findings, based on research in mice and in human cells, are reported Nov. 22 in Cell. The research adds an important piece to the long-standing puzzle of itch and helps explain why common skin conditions like eczema and atopic dermatitis are often accompanied by persistent itch.

In such conditions, the equilibrium of microorganisms that keep our skin healthy is often thrown off balance, allowing S. aureus to flourish, the researchers said. Up until now, the itch that occurs with eczema and atopic dermatitis was believed to arise from the accompanying inflammation of the skin. But the new findings show that S. aureus single-handedly causes itch by instigating a molecular chain reaction that culminates in the urge to scratch.

“We’ve identified an entirely novel mechanism behind itch — the bacterium Staph aureus, which is found on almost every patient with the chronic condition atopic dermatitis. We show that itch can be caused by the microbe itself,” said senior author Isaac Chiu, associate professor of immunology in the Blavatnik Institute at HMS.

The study experiments showed that S. aureus releases a chemical that activates a protein on the nerve fibers that transmit signals from the skin to the brain. Treating animals with an FDA-approved anti-clotting medicine successfully blocked the activation of the protein to interrupt this key step in the itch-scratch cycle. The treatment relieved symptoms and minimized skin damage.

The findings can inform the design of oral medicines and topical creams to treat persistent itch that occurs with various conditions linked to an imbalance in the skin microbiome, such as atopic dermatitis, prurigo nodularis, and psoriasis.

The repeated scratching that is a hallmark of these conditions can cause skin damage and amplify inflammation.

“Itch can be quite debilitating in patients who suffer from chronic skin conditions. Many of these patients carry on their skin the very microbe we’ve now shown for the first time can induce itch,” said study first author Liwen Deng, a postdoctoral research fellow in the Chiu Lab.

Identifying the molecular spark plug that ignites itch

Researchers exposed the skin of mice to S. aureus. The animals developed intensifying itch over several days, and the repeated scratching caused worsening skin damage that spread beyond the original site of exposure.

Moreover, mice exposed to S. aureus became hypersensitive to innocuous stimuli that would not typically cause itch. The exposed mice were more likely than unexposed mice to develop abnormal itching in response to a light touch.

This hyperactive response, a condition called alloknesis, is common in patients with chronic conditions of the skin characterized by persistent itch. But it can also happen in people without any underlying conditions — think of that scratchy feeling you might get from a wool sweater.

To determine how the bacterium triggered itch, the researchers tested multiple modified versions of the S. aureus microbe that were engineered to lack specific pieces of the bug’s molecular makeup. The team focused on 10 enzymes known to be released by this microbe upon skin contact. One after another, the researchers eliminated nine suspects — showing that a bacterial enzyme called protease V8 was single-handedly responsible for initiating itch in mice. Human skin samples from patients with atopic dermatitis also had more S. aureus and higher V8 levels than healthy skin samples.

The analyses showed that V8 triggers itch by activating a protein called PAR1, which is found on skin neurons that originate in the spinal cord and carry various signals — touch, heat, pain, itch — from the skin to the brain. Normally, PAR1 lies dormant but upon contact with certain enzymes, including V8, it gets activated. The research showed that V8 snips one end of the PAR1 protein and awakens it. Experiments in mice showed that once activated, PAR1 initiates a signal that the brain eventually perceives as itch. When researchers repeated the experiments in lab dishes containing human neurons, they also responded to V8.

Interestingly, various immune cells implicated in skin allergies and classically known to cause itch — mast cells and basophils — did not drive itch after bacterial exposure, the experiments showed. Nor did inflammatory chemicals called interleukins, or white cells, which are activated during allergic reactions and are also known to be elevated in skin diseases and even in certain neurologic disorders.

“When we started the study, it was unclear whether the itch was a result of inflammation or not,” Deng said. “We show that these things can be decoupled, that you don’t necessarily have to have inflammation for the microbe to cause itch, but that the itch exacerbates inflammation on the skin.”

Interrupting the itch-scratch cycle

Because PAR1 — the protein activated by S. aureus — is involved in blood-clotting, researchers wanted to see whether an already approved anticlotting drug that blocks PAR1 would stop itch. It did.

The itchy mice whose skin was exposed to S. aureus experienced rapid improvement when treated with the drug. Their desire to scratch diminished dramatically, as did the skin damage caused by scratching.

Moreover, once treated with PAR1 blockers, the mice no longer experienced abnormal itch in response to innocuous stimuli.

The PAR1 blocker is already used in humans to prevent blood clots and could be repurposed as anti-itch medication. For example, the researchers noted, the active ingredient in the medicine could become the basis for anti-itch topical creams.

One immediate question that the researchers plan to explore in future work is whether other microbes besides S. aureus can trigger itch.

“We know that many microbes, including fungi, viruses, and bacteria, are accompanied by itch but how they cause itch is not clear,” Chiu said.

Beyond that, the findings raise a broader question: Why would a microbe cause itch? Evolutionarily speaking, what’s in it for the bacterium?

One possibility, the researchers said, is that pathogens may hijack itch and other neural reflexes to their advantage. For example, previous research has shown that the TB bacterium directly activates vagal neurons to cause cough, which might enable it to spread more easily from one host to another.

“It’s a speculation at this point, but the itch-scratch cycle could benefit the microbes and enable their spread to distant body sites and to uninfected hosts,” Deng said. “Why do we itch and scratch? Does it help us, or does it help the microbe? That’s something that we could follow up on in the future.”

The work was funded by the National Institutes of Health (grants R01AI168005, R01AI153185, R01NS065926, R01NS102161, R01NS111929, R37AI052453, R01AR076082, U01AI152038, UM1AI151958, R01AI153185, R01JL160582, F32AI172080, T32AI049928, 1R21AG075419), Food Allergy Science Initiative (FASI), Burroughs Wellcome Fund, Drako Family Fund, Jackson-Wijaya Research Fund, Canadian Institutes of Health Research (CIHR) (grants 376560 and 469411), and ANR-PARCURE (PRCE-CE18, 2020).

Chiu serves on the scientific advisory board of GSK Pharmaceuticals. Provisional patent application Serial No. 63/438,668, in which some coauthors are listed as inventors, was filed based on these findings.

The cells, with a size twice the thickness of a strand of hair, have significant advantages over conventional solar technologies, reducing electrode-induced shadowing by 95% and potentially lowering energy production costs by up to three times.

The technological breakthrough — led by Mathieu de Lafontaine, a postdoctoral researcher at the University of Ottawa and a part-time physics professor; and Karin Hinzer, vice-dean, research, and University Research Chair in Photonic Devices for Energy at the Faculty of Engineering — paves the way for a new era of miniaturization in the field of electronic devices.

The micrometric photovoltaic cell manufacturing process involved a partnership between the University of Ottawa, the Université de Sherbrooke in Quebec and the Laboratoire des Technologies de la Microélectronique in Grenoble, France.

“These micrometric photovoltaic cells have remarkable characteristics, including an extremely small size and significantly reduced shadowing. Those properties lend themselves to various applications, from densification of electronic devices to areas such as solar cells, lightweight nuclear batteries for space exploration and miniaturization of devices for telecommunications and the internet of things,” Hinzer says.

A breakthrough with huge potential

“This technological breakthrough promises significant benefits for society. Less expensive, more powerful solar cells will help accelerate the energy shift. Lightweight nuclear batteries will facilitate space exploration, and miniaturization of devices will contribute to the growth of the internet of things and lead to more powerful computers and smartphones,” de Lafontaine says.

“The development of these first back-contact micrometric photovoltaic cells is a crucial step in the miniaturization of electronic devices,” he adds.

“Semiconductors are vital in the shift to a carbon-neutral economy. This project is one of many research initiatives that we’re undertaking at the Faculty of Engineering to achieve our societal goals,” says Hinzer. Semiconductors are included in three of the five research areas at the Faculty of Engineering, namely, information technologies, photonics and emerging materials, and two of the four strategic areas of research at the University of Ottawa, namely, creating a sustainable environment and shaping the digital world.

This international partnership between Canada and France illustrates the importance of innovation and research in micromanufacturing, leading the way to a future in which technology will become more powerful and accessible than ever. It also marks an historic step in the evolution of the global scientific and technology scene.

This initiative was funded by the Natural Sciences and Engineering Research Council of Canada, the Fonds de recherche du Québec Nature et technologies, the Horizon Europe Framework program, Prompt Québec and STACE Inc.

One chemical used in some anti-cancer drugs, for example, costs pharmaceutical companies $3,200 per gram — 50 times more than a gram of gold. The UCLA researchers devised an inexpensive way to produce this drug molecule from a chemical costing just $3 per gram. They were also able to apply the process to produce many other chemicals used in medicine and agriculture for a fraction of the usual cost.

This feat, published in the journal Science, involves a process known as “aminodealkenylation.” Using oxygen as a reagent and copper as a catalyst to break the carbon-carbon bonds of many different organic molecules, the researchers replaced these bonds with carbon-nitrogen bonds, converting the molecules into derivatives of ammonia called amines.

Because amines interact strongly with molecules in living plants and animals, they are widely used in pharmaceuticals, as well as in agricultural chemicals. Familiar amines include nicotine, cocaine, morphine and amphetamine, and neurotransmitters like dopamine. Fertilizers, herbicides and pesticides also contain amines.

Industrial production of amines is therefore of great interest, but the raw materials and reagents are often expensive, and the processes can require many complicated steps to complete. Using fewer steps and no expensive ingredients, the process developed at UCLA can produce valuable chemicals at a much lower cost than current methods.

“This has never been done before,” Kwon said. “Traditional metal catalysis uses expensive metals such as platinum, silver, gold and palladium, and other precious metals such as rhodium, ruthenium and iridium. But we are using oxygen and copper, one of the world’s most abundant base metals.”

The new method uses a form of oxygen called ozone, a potent oxidant, to break the carbon-carbon bond in hydrocarbons called alkenes, and a copper catalyst to couple the broken bond with nitrogen, turning the molecule into an amine. In one example, the researchers produced a c-Jun N-terminal kinase inhibitor — an anti-cancer drug — in just three chemical steps, instead of the 12 or 13 steps previously needed. The cost per gram can thus be reduced from thousands of dollars to just a few dollars.

In another example, the protocol took just one step to convert adenosine — a neurotransmitter and DNA building block that costs less than 10 cents per gram — into the amine N6-methyladenosine. The amine plays crucial roles in controlling gene expression in cellular, developmental and disease processes, and its production cost has previously been $103 per gram.

Kwon’s research group was able to modify hormones, pharmaceutical reagents, peptides and nucleosides into other useful amines, showing the new method’s potential to become a standard production technique in drug manufacturing and many other industries.

The research was funded by the National Institutes of Health.

“The use of an AED is the single most important factor in saving lives. We have been deploying drones equipped with AED since the summer of 2020 and show in this follow-up study that drones can arrive at the scene before an ambulance by several minutes. This lead time has meant that the AED could be used by people at the scene in several cases,” says Andreas Claesson, Associate Professor at the Center for Cardiac Arrest Research at the Department of Clinical Research and Education, Södersjukhuset, Karolinska Institutet, and principal investigator of the study.

Every year, around 6000 people in Sweden suffer a sudden cardiac arrest, but only a tenth of those affected survive. Although an early shock with a AED can dramatically increase the chance of survival and there are tens of thousands of AED in the community, they are not available in people’s homes where most cardiac arrests occur.

To shorten the time to defibrillation with an AED, Karolinska Institutet, together with Region Västra Götaland, SOS Alarm and the drone operator Everdrone, has since 2020 tested the possibility of sending out a drone with a AED at the same time as an ambulance is alerted. The project covered an area of approximately 200,000 people in western Sweden. An initial study conducted in the summer of 2020 in Gothenburg and Kungälv showed that the idea was feasible and safe.

“This more comprehensive and follow-up study now shows in a larger material that the methodology works throughout the year, summer and winter, in daylight and darkness. Drones can be alerted, arrive, deliver AED, and people on site have time to use the AED before the ambulance arrives,” says Sofia Schierbeck, PhD student at the same department and first author of the study.

In the study, drones delivered a AED in 55 cases of suspected cardiac arrest. In 37 of these cases, the delivery took place before an ambulance, corresponding to 67 percent, with a median lead of 3 minutes and 14 seconds. In the 18 cases of actual cardiac arrest, the caller managed to use the AED in six cases, representing 33 percent. A shock was recommended by the device in two cases and in one case the patient survived.

“Our study now shows once and for all that it is possible to deliver AED with drones and that this can be done several minutes before the arrival of the ambulance in connection with acute cardiac arrest,” says Andreas Claesson. “This time saving meant that the healthcare emergency center could instruct the person who called the ambulance to retrieve and use the AED in several cases before the ambulance arrived.”

The research was mainly funded by the Swedish Heart-Lung Foundation.

Hikikomori is a condition characterized by sustained physical isolation or social withdrawal for a period exceeding six months. It was first defined in Japan in 1998, and while thought to be a Japan specific ‘culture-bound’ syndrome, recent evidence has shown a marked growth of it worldwide. Researchers and medical professionals also fear that the recent COVID-19 pandemic has compounded the increase of hikikomori patients across the globe.

However, there is yet to be a standardized tool to identify the hikikomori pathology. The new HiDE assessment tool, developed by Associate Professor Takahiro A. Kato of the Graduate School of Medical Sciences published in World Psychiatry, is intended to be the next step in a transcultural tool to help identify and assess hikikomori individuals.

In 2013, the Kyushu University hospital established the world’s first outpatient clinic for hikikomori in the hopes to research the pathology and find better methods of treatment. Over the years, Kato and his team have developed different methods for early detection of hikikomori and has even been investigating possible biomarkers of the pathology.

“HiDE is a questionnaire we’ve been developing at our clinic at the University Hospital. We’ve refined it over the years, and today it takes roughly 5-20 minutes to complete depending on the answers,” explains Kato. “It’s primarily divided into two sections. The first section looks at the features of the patient’s behavior to see if they exhibit hikikomori. The second section is used to help us gain context to the patient’s extent of social withdrawal.”

The team has also added a screening form to the HiDE in case clinicians lack the time to administer the entire tool. They suggest that the full questionnaire be administered to patients who respond that they ‘spend one hour or less per day out of their home, at least three days a week’ and that ‘their family, others, or are personally bothered by this.’

“The HiDE has proven to be an indispensable tool for the structured assessment of pathological social withdrawal in our clinical practice and research. But more empirical studies must be done to assess its validity beyond our practice,” concludes Kato. “We would like to see this used by our colleagues around the world, so we can work to refine the tool. Hikikomori is becoming a global phenomenon, and a collective effort in recognizing and treating hikikomori is going to be vital.”

It is well known that patients with rheumatoid arthritis are at increased risk of autoimmune thyroid diseases such as Hashimoto’s disease and Graves’ disease. While patients with RA are usually treated with immunomodulatory drugs that affect the immune system, such drugs are rarely used in autoimmune thyroid diseases. Instead, such patients are treated with thyroid hormone to compensate for the changes in normal thyroid function that accompany autoimmune thyroid disease.

The researchers in the current study wanted to investigate whether immunomodulatory drugs that reduce inflammation in the joints of patients with RA might also reduce the risk of these patients developing autoimmune thyroid disease. Previous studies in mice suggest that so-called DMARDs, a type of immune-modulatory drugs used to treat rheumatoid arthritis, can reduce inflammation in the thyroid gland. Still, knowledge of whether this effect also applies to humans is limited, according to the research team.

The researchers used data between 2006 and 2018 on over 13,000 patients with rheumatoid arthritis and their treatment, as well as data from over 63,000 individuals in a matched control group without rheumatoid arthritis.

The researchers found that the risk of developing an autoimmune thyroid disease among RA patients was lower after their onset of the rheumatic disease than before diagnosis.

The most pronounced reduction in the risk of autoimmune thyroid disease was seen in patients with rheumatoid arthritis treated with immunomodulatory drugs or ‘biological DMARDs’. In these patients, the risk of autoimmune thyroid disease was 46 percent lower than in the control group without rheumatoid arthritis.

“These results support the hypothesis that certain types of immunomodulatory drugs could have a preventive effect on autoimmune thyroid disease,” says Kristin Waldenlind, researcher at the Department of Medicine, Solna, Division of Clinical Epidemiology, Karolinska Institutet, specialist in rheumatology at Karolinska University Hospital and first author of the study. She continues:

“Our results do not prove that it is the treatment with immunomodulatory drugs that led to the reduced risk of autoimmune thyroid disease, but provide support for this hypothesis. The results, if they can be replicated in further studies, open up the possibility of studying more directly in clinical trials whether the immunomodulatory drugs currently used for rheumatoid arthritis could also be used for the early treatment of autoimmune thyroid disease, i.e. for new areas of use of these drugs, known as drug repurposing.

The Swedish Research Council, the Swedish Heart-Lung Foundation and Vinnova mainly financed the study.

There’s a popular saying in some circles that “a calorie is a calorie,” but science shows that it may not be true. In fact, it may be possible to eat more of some kinds of calories while also improving your health.

“We like to say a calorie is not just a calorie,” says Dudley Lamming, a professor and metabolism researcher at the University of Wisconsin School of Medicine and Public Health. “Different components of your diet have value and impact beyond their function as a calorie, and we’ve been digging in on one component that many people may be eating too much of.”

Lamming is the lead author of a new study in mice, published recently in the journal Cell Metabolism, showing that cutting down the amount of a single amino acid called isoleucine can, among other benefits, extend their lifespan, make them leaner and less frail as they age and reduce cancer and prostate problems, all while the mice ate more calories.

Amino acids are the molecular building blocks of proteins, and Lamming and his colleagues are interested in their connection to healthy aging.

In earlier research, data from UW-Madison’s Survey of the Health of Wisconsin showed the scientists that Wisconsinites with higher body mass index measurements (higher is more overweight or obese) tend to consume more isoleucine, an essential amino acid everyone needs to eat. Isoleucine is plentiful in foods including eggs, dairy, soy protein and many kinds of meat.

To better understand its health effects, Lamming and collaborators from across disciplines at UW-Madison fed genetically diverse mice either a balanced control diet, a version of the balanced diet that was low in a group of about 20 amino acids, or a diet formulated to cut out two-thirds of the diet’s isoleucine. The mice, which began the study at about 6 months of age (equivalent to a 30-year-old person) got to eat as much as they wanted.

“Very quickly, we saw the mice on the reduced isoleucine diet lose adiposity — their bodies got leaner, they lost fat,” says Lamming, while the bodies of the mice on the low-amino-acid diet also got leaner to start, but eventually regained weight and fat.

Mice on the low-isoleucine diet lived longer — on average 33% longer for males and 7% longer for females. And, based on 26 measures of health, including assessments ranging from muscle strength and endurance to tail use and even hair loss, the low-isoleucine mice were in much better shape during their extended lives.

“Previous research has shown lifespan increase with low-calorie and low-protein or low-amino-acid diets starting in very young mice,” says Lamming, whose work is supported by the National Institutes of Health. “We started with mice that were already getting older. It’s interesting and encouraging to think a dietary change could still make such a big difference in lifespan and what we call ‘healthspan,’ even when it started closer to mid-life.”

The mice on the low-isoleucine diets chowed down, eating significantly more calories than their study counterparts — probably to try to make up for getting less isoleucine, according to Lamming. But they also burned far more calories, losing and then maintaining leaner body weights simply through adjustments in metabolism, not by getting more exercise.

At the same time, Lamming says, they maintained steadier blood sugar levels and male mice experienced less age-related prostate enlargement. And while cancer is the leading cause of death for the diverse strain of mice in the study, the low-isoleucine males were less likely to develop a tumor.

Dietary amino acids are linked to a gene called mTOR that appears to be a lever on the aging process in mice and other animals as well as to a hormone that manages the body’s response to cold and has been considered a potential diabetes drug candidate for human patients. But the mechanism behind the stark benefits of low-isoleucine intake is not well understood. Lamming thinks the new study’s results may help future research pick apart causes.

“That we see less benefit for female mice than male mice is something we may be able to use to get to that mechanism,” he says.

While the results are promising, humans do need isoleucine to live. And winnowing a significant amount of isoleucine out of a diet that hasn’t been preformulated by a mouse chow company is not an easy task.

“We can’t just switch everyone to a low-isoleucine diet,” Lamming says. “But narrowing these benefits down to a single amino acid gets us closer to understanding the biological processes and maybe potential interventions for humans, like an isoleucine-blocking drug.”

The Survey of the Health of Wisconsin showed that people vary in isoleucine intake, with leaner participants tending to eat a diet lower in isoleucine. Other data from Lamming’s lab suggest that overweight and obese Americans may be eating significantly more isoleucine than they need.

“It could be that by choosing healthier foods and healthier eating in general, we might be able to lower isoleucine enough to make a difference,” Lamming says.

This research was funded in part by grants from the National Institutes of Health (AG056771, AG062328, AG081482, AG084156, DK125859, F31AG066311, R01AG062328-03S1, F31AG081115, F31AG082504, T32AG000213, F32AG077916, RF1AG056771-06S1, K01AG059899, R01DK133479, P30DK020579, K12HD101368, R01AA029124, P30 CA014520, P50DE026787, U54DK104310, R01DK131175 and P30CA014520) and the U.S. Department of Veterans Affairs (I01-BX004031).

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.

The team plans to investigate those interactions, seeking to better understand how taste signals from food interact with feedback from the gut to suppress our appetite during a meal.