Researchers have identified brain cells in mice that promote weight loss.
In a groundbreaking discovery, a team of Swedish researchers led by Julia Teixidor-Deurolfeu from the University of Gothenburg have identified a specific group of neurons in the brainstem that plays a pivotal role in mediating the weight loss and appetite suppression effects of semaglutide, a popular weight loss drug, without causing the unpleasant side effects like nausea that often accompany such medication.
The study, published in ScienceDirect, aims to shed light on how the brain regulates hunger and satiety, and how targeting these mechanisms could lead to the development of new obesity treatment methods with minimal side effects.
Conducted at the University of Gothenburg, the research centered on neurons in the area postrema (AP) and nucleus of the solitary tract (NTS), both located in the brainstem. The scientists found that many of these neurons expressed the Adcyap1 gene, and were directly activated by semaglutide. When these neurons were activated, there was a significant decrease in appetite and weight, but no accompanying feelings of nausea.
Remarkably, the researchers were able to achieve this effect by activating these neurons without the use of the drug itself. They employed a method called chemogenetic activation, which allowed them to stimulate these neurons directly, resulting in impressive weight loss without any unwanted sensations. Furthermore, when these neurons were removed, the action of semaglutide weakened, confirming their key role in this process.
The team's findings hold great promise for the future of obesity treatment. By selectively targeting these Adcyap1+ neurons in the brainstem, drugs like semaglutide could be developed that focus on appetite reduction and weight loss, while minimizing or eliminating the unpleasant side effects commonly associated with current medications.
Understanding the mechanism by which these neurons function will help researchers gain a better insight into how the brain regulates hunger and satiety. This could pave the way for the development of new and improved obesity treatment methods in the future.
(Enrichment Data Relevance Note: The enrichment data provides additional scientific details about the mechanism of action, key findings, and implications of the study, which have been integrated into the article to provide a more comprehensive understanding of the research.)
- The groundbreaking study in ScienceDirect highlights the potential of targeting health-and-wellness through science, specifically by focusing on neurons in the brainstem that express the Adcyap1 gene, as they play a crucial role in managing weight through therapies-and-treatments like semaglutide.
- The researchers at the University of Gothenburg discovered that these neurons, located in the area postrema (AP) and nucleus of the solitary tract (NTS), are activated by semaglutide, leading to a reduction in appetite and weight, without causing the adverse medical-conditions like nausea.
- The advancements in nutrition and weight-management could benefit greatly from this research, as it opens up opportunities for developing new drugs that primarily focus on appetite suppression and weight loss, minimizing the unwanted side effects traditionally associated with weight loss medications.
