RT @SinghArashdeep: New in @jclinicalinvest .We identified GLP-1 receptor therapy as a promising Bardet-Biedl Syndrome #BBS treatment. 🔬 We….

Very nice work providing direct evidence that microbiota in the gut talk with the host via the vagus nerve.

Generate videos in just a few seconds. Try Grok Imagine, free for a limited time.

RT @pipethero: Delighted to highlight new work by Kelly Jameson and colleagues showing that select microbial metabolites in the small intes….

RT @SSIBsociety: 📢 SSIB 2025 Annual Meeting.📍 Oxford, UK | 🗓 July 28–Aug 1.🌟 5 Days of Science, Networking, & Fun!. Keynotes: Sadaf Farooqi….

RT @egkrause_gsu: Excited by our latest joint production discovering body-to-brain communication that controls whole body metabolism. It wa….

RT @zenbrainest: Chemogenetic excitation of NGOxtr creates patterns of brain activity associated with augmented hypothalamic–pituitary–adr….

@mhrebecaaa @KElsaafien @javstern @scientistcaitb and twitterless Karen Scott, Dominique Johnson, Matthew Krichner, Sophia Eikenberry and Jessica Sa.

This work wouldn't have been possible without fellow corresponding authors @egkrause, and twitterless Annette deKloet. Huge thank you to all involved. We’d love to hear your thoughts! How do you see this being applied in the real world? Reply below! ⬇️.

Our findings could inspire new strategies for:. -Obesity therapies that mimic this natural fat-burning state. -Stress management, linking fear, hunger, and metabolic conservation. -Space travel, enabling resource-efficient survival in harsh environments 🚀.

Unlike our food memory paper, which focused on gut-mediated nutrient-specific learning, this work reveals how mechanosensors link physiological states to energy-saving mechanisms like torpor. Two different papers. Two different discoveries. One shared focus: the gut-brain axis.

This state mimics hibernation, but here’s what’s exciting:. Repeated activation of NGOxtr neurons caused sustained fat loss without rebound overeating, even on a high-fat diet. Fat mass decreased while lean mass was preserved, making this mechanism a potential obesity treatment.

Here, we activated vagal neurons expressing oxytocin receptor (NGOxtr). These neurons sense stretch in the gut, and aortic arch, and send powerful signals to the brain, triggering:. 🌡️ Reduced body temperature.❤️ Slower heart rate.🫁 Lower energy expenditure.🍽️ Suppressed hunger.

Imagine a mouse that’s hungry but senses a predator outside its burrow. Leaving to forage is too risky, but staying put burns precious energy. Enter the torpor-like state: a survival mechanism that conserves energy, suppresses hunger, and allows the mouse to wait out the danger.

While central circuits of torpor are well-studied, this is the first demonstration that peripheral circuits, specifically vagal mechanosensors in the heart and gut, can trigger this state independently. Here’s why this matters ⬇️.

Thrilled to share our second paper in two days, published today in #NatureMetabolism!. Yesterday, we explored food memory. Today, we reveal something entirely different: peripheral vagal circuits can induce a torpor-like state in mice. 🧵.

RT @zhang_chuchu: First review from the lab on nausea and area postrema:.

RT @MonellSc: 🧵 Can memory influence what and how much we eat?. Short answer is yes!. Memory is often overlooked as a key driver of food in….

Read the full study here: �.And if you’d like to know more, feel free to reach out!.

Huge thanks to our amazing team lead by superstar graduate student @mingxin_yang. This work was supported by @NIH and @American_Heart. Collaboration made it possible @MonellSc @USC! 🤝.

This research opens up exciting possibilities: Could we disrupt the memory triggers that drive overeating in today’s obesogenic environment? Stay tuned for more studies exploring these pathways! 🧠🍽️.