The fight against obesity has been an ongoing battle for decades. With over one billion people worldwide affected by this condition, scientists are constantly seeking new and effective treatments. Recently, researchers at the Salk Institute have made a groundbreaking discovery that could potentially change the game. They’ve identified a tiny molecule called Adipocyte-smORF-1183, which plays a crucial role in regulating fat cell biology and lipid accumulation.

This breakthrough was made possible by using CRISPR gene editing to screen thousands of fat cell genes. The researchers found dozens of genes that likely code for microproteins involved in either fat cell proliferation or lipid accumulation. One of these potential microproteins, Adipocyte-smORF-1183, was verified to influence lipid droplet formation in fat cells.

The discovery of this molecule is a significant step towards understanding the complex energy storage system in our bodies. It also opens up new possibilities for developing targeted therapies that can specifically address obesity and related metabolic disorders.

While more research is needed to fully understand the implications of Adipocyte-smORF-1183, this breakthrough is a promising development in the fight against obesity. As scientists continue to study this molecule and its role in fat cell biology, we may see new and innovative treatments emerge that can help millions of people worldwide manage their weight and improve their overall health.

In related news, researchers at Scripps Research Institute have also been studying microproteins involved in fat cell differentiation and proliferation. Their work has identified several potential candidates for further investigation, which could lead to new therapeutic targets for obesity and metabolic disorders.

The study was supported by various grants from the National Institutes of Health, Ferring Foundation, Clayton Foundation, and Larry and Carol Greenfield Technology Fund. Further validation or screening of new cell libraries will expand the list of potential drug candidates, setting the stage for the new-and-improved obesity and metabolic disorder therapeutics of the future.

Scientists have made a groundbreaking discovery that could revolutionize the way we approach weight loss. A multidisciplinary team led by Robert Doyle, a chemistry professor at Syracuse University, has identified a hidden brain shortcut that can help people lose weight without experiencing nausea, a common side effect of current weight loss medications.

Current weight loss and diabetes drugs often target brain neurons that control appetite but frequently cause unpleasant side effects like nausea and vomiting. In fact, 70% of patients stop treatment within a year due to these side effects. Doyle’s team has been researching alternative targets for treating obesity and diabetes, looking beyond neurons to study “support” cells such as glia and astrocytes.

The research team discovered that support cells in the hindbrain naturally produce a molecule named octadecaneuropeptide (ODN), which suppresses appetite. In lab tests, injecting ODN directly into rats’ brains made them lose weight and improve how they processed glucose. However, injecting directly into the brain isn’t a practical treatment for people.

To overcome this limitation, researchers created a new version of the molecule named tridecaneuropeptide (TDN), which could be given to human patients through regular injections akin to today’s Ozempic or Zepbound. When tested in obese mice and musk shrews, TDN helped the animals lose weight and respond better to insulin without causing nausea or vomiting.

One goal of the research team is to produce weight loss without aiming new therapeutic molecules at neurons. The new TDN molecule bypasses neurons, taking a shortcut to directly target support cells, which researchers found also produce appetite suppression. This approach has the potential to reduce the unpleasant side effects caused by GLP-1 drugs.

“The idea is to start the process halfway through, reducing the marathon of chemical reactions and negative side effects,” says Doyle. “If we could hit that downstream process directly, then potentially we wouldn’t have to use GLP-1 drugs with their side effects. Or we could reduce their dose, improving the toleration of these drugs.”

A new company called CoronationBio has been launched to turn this discovery into a real-world treatment. The company has licensed intellectual property related to ODN derivatives for the treatment of obesity and cardio-metabolic disease from Syracuse University and the University of Pennsylvania.

Their focus is on translating candidates into the clinic, aiming to start human trials in 2026 or 2027. This breakthrough has the potential to revolutionize the way we approach weight loss, providing a more comfortable and effective solution for millions of people worldwide.

Breaking Barriers in Diabetic Wound Healing: A Revolutionary “Smart” Gel Accelerates Blood Flow and Restores Tissue Repair

Chronic diabetic wounds, particularly diabetic foot ulcers, pose a significant burden for patients due to impaired blood vessel growth and subsequent tissue repair issues. A groundbreaking study has unveiled a novel approach by combining small extracellular vesicles (sEVs) loaded with miR-221-3p and a GelMA hydrogel to target thrombospondin-1 (TSP-1), a protein that suppresses angiogenesis. This innovative bioactive wound dressing not only accelerates healing but also promotes blood vessel formation, offering a promising new approach to treating one of the most challenging complications of diabetes.

The study explores a new method to stimulate angiogenesis and speed up the healing process by targeting TSP-1 with miR-221OE-sEVs encapsulated in GelMA. This engineered hydrogel has shown significant enhancement in wound healing and blood vessel formation in diabetic mice, offering hope for more effective treatments in the future.

Researchers discovered that high glucose conditions commonly found in diabetic wounds lead to increased levels of TSP-1 in endothelial cells, impairing their ability to proliferate and migrate – key processes for angiogenesis. By utilizing miR-221-3p, a microRNA that targets and downregulates TSP-1 expression, they restored endothelial cell function. The engineered miR-221OE-sEVs were encapsulated within a GelMA hydrogel, ensuring a controlled release at the wound site.

In animal trials, this composite dressing dramatically accelerated wound healing, with a notable increase in vascularization and a 90% wound closure rate within just 12 days, compared to slower healing in control groups. This breakthrough has significant implications for diabetic wound care, offering patients more efficient and lasting wound healing solutions.

As further research and clinical trials progress, the promise of combining miRNA-based therapies with biocompatible hydrogels could become a cornerstone in regenerative medicine, opening up possibilities beyond diabetic foot ulcers. The technology could be adapted for use in treating other chronic wounds, such as those caused by vascular diseases, or even in regenerating tissues like bone and cartilage.