Your colon's got a ‘sixth sense' — here's how it can lead to weight loss
New research from Duke University highlights the role of neuropods, specialized sensory cells in the colon that act like taste buds for the gut.
Neuropods 'sample' nutrients like sugars and bacterial byproducts and quickly send signals to the brain, guiding food choices and even influencing when it's time to stop eating.
Researchers call the phenomenon 'neurobiotic sense' — a 'hidden sixth sense.' They hope it paves the way for new obesity treatments and provides insight into mental health disorders affected by diet.
'It's similar to how we use our other senses — sight, sound, smell, taste and touch — to interpret our world,' the study authors said. 'But this one operates from an unexpected place: The gut.'
Scientists have long known about the gut-brain connection, the major communication highway that affects digestion, mood and overall well-being.
For their part, the colon's neuropod cells can warn the brain of bacterial intruders.
The new Duke study — published Wednesday in the journal Nature — focuses on flagellin, a key structural protein that enables bacteria to move.
Some of our gut bacteria release flagellin when we eat.
Neuropod cells use a special receptor called TLR5 to recognize flagellin and relay the information through the vagus nerve — the main link between the gut and the brain.
The researchers examined how this works in mice.
They had one set of mice fast overnight before giving them a small dose of flagellin from Salmonella Typhimurium, a well-studied type of bacteria that causes infections. The mice ate less.
They repeated these steps with mice that had their TLR5 receptor 'knocked out.' These mice continued to eat and ended up gaining weight because the brain couldn't pick up on the flagellin signal.
No other changes to the mice's behavior were detected.
The results suggest that TLR5 helps tell the brain that it's time to put down the fork. The brain doesn't get the memo without the receptor.
'If we disrupt this pathway, then the animals end up eating a little bit more for a little bit longer,' Duke School of Medicine neuroscientist Diego Bohórquez told The Post.
Bohórquez previously demonstrated that neuropod cells in the gut can distinguish between real sugar and artificial sweeteners.
The cells communicate this information to the brain, driving the preference for sugar.
'Looking ahead, I think this work will be especially helpful for the broader scientific community to explain how our behavior is influenced by microbes,' said Bohórquez, a professor of medicine and neurobiology and senior study author.
'One clear next step is to investigate how specific diets change the microbial landscape in the gut,' he added. 'That could be a key piece of the puzzle in conditions like obesity or psychiatric disorders.'
Bohórquez said that future research should also address the effect of bacterial strains beyond Salmonella Typhimurium and explore whether antibiotics or probiotics can influence this neurobiotic sense.
Solve the daily Crossword
Hashtags

Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles


Gizmodo
2 days ago
- Gizmodo
Physicists Create First-Ever Antimatter Qubit, Making the Quantum World Even Weirder
Readers following our existential physics coverage may remember a recent breakthrough from CERN concerning matter's evil twin, antimatter. An outstanding mystery in physics is that our universe contains more matter than antimatter, contradicting most theoretical predictions. Scientists, therefore, understandably want to explain why and how this is the case. CERN announced yet another significant leap for studying antimatter—and this time, the achievement creeps into the realm of quantum computing. In a Nature paper published on July 23, CERN's Baryon Antibaryon Symmetry Experiment (BASE) collaboration announced the first-ever demonstration of an antimatter quantum bit, or qubit—the smallest unit of information for quantum computers. The qubit in question is an antiproton, a proton's antimatter counterpart, caught in a curious quantum swing—arcing back and forth between 'up' and 'down' spin states in perfect rhythm. The oscillation lasted for 50 seconds. The technical prowess that enabled this result represents a significant leap forward in our understanding of antimatter, the researchers claim. For the experiment, the team applied a technique called coherent quantum transition spectroscopy, which measures—with chilling precision—a particle's magnetic moment, or its behavior inside magnetic fields. First, the team brought in some antiprotons from CERN's antimatter factory, trapping the particles in an electromagnetic Penning trap—a superposition of magnetic fields. Next, they set up a second multi-trap inside the same magnet, extracting individual antiprotons to measure and tweak the particle's spin states in the process. Quantum states are fragile and easily disturbed by outside distractions. The wrong push can immediately send them spiraling down the drain toward decoherence—at which point the system loses the valuable information physicists hope to find. This fundamental limitation of quantum systems was a major concern for the BASE collaboration, who in 2017 used a similar setup to the new experiment to confirm that protons and antiprotons had practically identical magnetic moments. The team made substantial revisions to its technology, paying special attention to developing the mechanisms needed to suppress and eliminate decoherence. This hard work paid off; the antiproton performed a stable quantum swing for 50 seconds—a motion akin to how qubits exist in superpositions of states, which theoretically could allow them to store exponential loads of information. Additionally, it marked the first time physicists observed this phenomenon in a single free nuclear magnetic moment, whereas previous experiments had only seen it in large groups of particles. 'This represents the first antimatter qubit and opens up the prospect of applying the entire set of coherent spectroscopy methods to single matter and antimatter systems in precision experiments,' BASE spokesperson Stefan Ulmer said in a statement. That said, the team doesn't believe the new results will introduce antimatter qubits to quantum computing, at least not anytime soon. 'It does not make sense to use [the antimatter qubit] at the moment for quantum computers, because, simply speaking, engineering related to production and storage of antimatter is much more difficult than for normal matter,' Latacz explained, adding that since matter and antimatter are known to share fundamental properties, opting for the latter wouldn't make practical sense. 'However, if in the future [we find] that antimatter behaves differently than matter, then it may be interesting to consider this.' There are additional improvements the team hopes to make, which will happen sometime very soon, Latacz said. The upgrades to BASE—termed BASE-STEP—will greatly improve our capacity to study antiprotons with higher precision and allow us to 'improve the measurement of the magnetic moment of the antiproton by at least a factor of 10, and in a longer perspective even a factor of 100,' she said. The new breakthrough could contribute to engineering advances in quantum computing, atomic clocks, and other areas. But as the researchers emphasize, such technological applications aren't anything we should expect any time soon. Nevertheless, the result itself presents some fascinating lessons for fundamental physics—questions that may take years to answer, but to quote physicist Sean Carroll from the other recent CERN finding, 'Well, it's a small part of a much bigger puzzle—but you know, every part matters.'

Engadget
3 days ago
- Engadget
CRISPR can stop malaria spread by editing a single gene in mosquitos
CRISPR gene-editing therapy has shown great potential to treat and even cure diseases, but scientists are now discovering how it can be used to prevent them as well. A team of researchers found a way to edit a single gene in a mosquito that prevented it from transmitting malaria, according to a paper published in Nature . These genetically modified mosquitos could eventually be released into the wild, helping prevent some of the 600,000 malaria deaths that occur each year. Mosquitos infect up to 263 million people yearly with malaria and efforts to reduce their populations have stalled as late. That's because both the mosquitos and their parasites that spread malaria have developed resistance to insecticides and other drugs. Now, biologists from UC San Diego, Johns Hopkins and UC Berkeley universities have figured out a way to stop malarial transmission by changing a single amino acid in mosquitos. The altered mosquitos can still bite people with malaria and pick up parasites from their blood, but those can no longer be spread to others. The system uses CRISPR-Cas9 "scissors" to cut out an unwanted amino acid (allele) that transmits malaria and replace it with a benign version. The undesirable allele, called L224, helps parasites swim to a mosquito's salivary glands where they can then infect a person. The new amino acid, Q224, blocks two separate parasites from making it to the salivary glands, preventing infection in people or animals. "With a single, precise tweak, we've turned [a mosquito gene component] into a powerful shield that blocks multiple malaria parasite species and likely across diverse mosquito species and populations, paving the way for adaptable, real-world strategies to control this disease," said researcher George Dimopoulos from Johns Hopkins University. Unlike previous methods of malarial control, changing that key gene doesn't affect the health or reproduction capabilities of mosquitos. That allowed the researchers to create a technique for mosquito offspring to inherit the Q224 allele and spread it through their populations to stop malarial parasite transmission in its tracks. "We've harnessed nature's own genetic tools to turn mosquitoes into allies against malaria," Dimopoulos said. If you buy something through a link in this article, we may earn commission.


New York Post
3 days ago
- New York Post
Llamas could help treat schizophrenia: study
Talk about a llama-zing discovery. They're known for their fluffy furs and sassy stares, but scientists have discovered that llamas may also be the key to treating schizophrenia. And this isn't even the first time this year that llamas have been at the heart of curing a scary health issue. Advertisement They're known for their fluffy furs and sassy stares, but it turns out llamas may also be the key to treating schizophrenia. Cavan for Adobe – In a mind-blowing new study, French researchers have developed a molecule from llama antibodies that could one day help patients with schizophrenia overcome cognitive deficits — a major hurdle that existing treatments fail to address. Scientists at the Institute of Functional Genomics in Montpellier have engineered what's called a nanobody — a tiny antibody fragment found in camelids like llamas — that can activate a specific glutamate receptor responsible for brain signaling. What's more, this molecule can cross the blood-brain barrier — a major challenge in drug development — and go straight to work on neural receptors when injected via a vein or muscle. Advertisement Researchers tested the llama-derived nanobody in two preclinical models of schizophrenia. Just one injection was enough to boost brainpower in mice, showing a clear and sustained improvement in cognitive function for up to a week. More research will be needed to see if this presents a promising new avenue of treatment for schizophrenia and, if so, whether or not this can be expanded to treat other psychiatric and neurodegenerative diseases. Advertisement The findings were published Wednesday in the journal Nature. Schizophrenia is a chronic mental disorder that affects how people perceive reality, leading to hallucinations, delusions, disorganized thinking and speech, paranoia and time gaps. elnariz – Schizophrenia is a chronic mental disorder that affects how people perceive reality, leading to hallucinations, delusions, disorganized thinking and speech, paranoia and time gaps. More than 200,000 people in the US are living with schizophrenia, for which there is no cure. Advertisement The cause of schizophrenia is still unknown, but research suggests a combination of genetic and environmental factors are likely to encourage its onset, which typically occurs between the ages of 16 and 30. Schizophrenia is primarily treated with antipsychotics, which target some of the more severe symptoms like hallucinations and delusions, but fail to do much for cognitive function. This new study offers hope for repairing cognition, as opposed to simply managing symptoms. 'In humans obviously we don't know [yet], but in mice yes, it is sufficient to treat most deficits of schizophrenia,' paper author and CNRS molecular biologist Jean-Philippe Pin told Newsweek. 'For development as a therapeutic tool, more safety and bioavailability studies are needed. Production of large quantities of high quality must be set up to start human studies. For these two possibilities, either a company takes up our project or we find investors to create a startup company.' Meanwhile, another study published last month found that llamas may also hold the secret weapon to curing COVID — and it's also in their nanobodies. 'This work provides a strong foundation for developing next-generation antibodies that could be vital in combating not only current but also future coronavirus threats,' said Dr. Xavier Saelens, senior author of the study and a principal investigator at the VIB-UGent Center for Medical Biotechnology in Belgium.