This technology identifies a fat-sensing pathway that can be targeted to modulate dietary fat preference, which can potentially be used to treat obesity, diabetes, and heart disease.
Obesity is caused by a caloric intake above the normal biological requirement and can predispose individuals to chronic diseases such as cardiovascular disease, diabetes, certain cancers, gastrointestinal conditions, chronic kidney disease, and musculoskeletal diseases. Upon food intake, enteroendocrine cells in the gut secrete hormones that facilitate appetite suppression by mediating neuronal signaling in the gut-brain axis. Consumption of high-fat foods can disrupt these neural circuits and lead to overeating. Current methods to treat obesity largely involve lifestyle changes, limited medicines, and weight-loss surgeries that have variable efficiencies as well as potential risks and side effects. Further study of fat-sensing pathways involved in the gut-brain axis can potentially identify specific therapeutic strategies for obesity and related chronic conditions.
This technology identifies a fat-sensing pathway that can be targeted to reduce appetite for high-fat foods and potentially treat obesity, diabetes, heart disease, and associated conditions. The technology involves two subsets of vagal sensory neurons that mediate nutrient and fat sensing which, upon ablation, can abolish dietary fat preference. The technology is specific, with no effects on preference for sugar and other essential nutrients. This technology can thus be used for the development of therapeutics to decrease appetite for the targeted treatment of obesity and associated chronic diseases.
This technology has been validated using rodent models.
Patent Pending (WO/2023/164661)
IR CU22137
Licensing Contact: Joan Martinez
