A groundbreaking study led by Dr. Zachary Knight, a professor of physiology at the University of California San Francisco, reveals that brain cells signaling the termination of eating are triggered by the taste of food rather than the fullness of the stomach. Published in the journal Nature, the research utilized novel brain imaging techniques to observe the caudal nucleus of the solitary tract (cNTS), a brainstem structure crucial for satiety, in awake mice. The study challenges conventional wisdom, showing that neurons, particularly prolactin-releasing hormone (PRLH) neurons, respond to taste stimuli, influencing the pace of ingestion. Unexpectedly, the findings suggest that the brainstem has two parallel pathways regulating eating speed and quantity. PRLH neurons, associated with non-aversive satiety, respond to taste rather than signals from the gut when food is ingested orally. The research sheds light on the brainstem’s ability to selectively attend to sensory cues, akin to the ‘cocktail party effect.’ Importantly, these insights have implications for treating obesity, as they align with the targets of Glucagon-like peptide 1 (GLP1) weight loss drugs. The study provides a foundation for understanding the neural mechanisms behind these drugs, potentially paving the way for more effective weight loss treatments. Additionally, the research explores the role of GLP1-related cells in inducing prolonged satiety, contributing to the drugs’ efficacy. The findings offer promising avenues for advancing our understanding of appetite regulation and improving obesity treatments.
Source: https://www.nejm.org/doi/full/10.1056/NEJMoa2307563?query=featured_home
