Poster #008
Genetic Differences Underlying Differential Responses to Semaglutide
Mentors: Jason Perez and Meaghan McCoy; Anna Kamitakahara, PhD
According to the CDC, nearly 40% of the US adult population is obese. Semaglutide (SEMA) – the active ingredient in drugs like Ozempic – is frequently used to treat obesity as it offers a more affordable, less invasive, and long-term alternative to traditional treatments such as bariatric surgery. However, 10-15% of SEMA users don’t lose weight at all. We hypothesize that differential responses to SEMA are due to genetic differences in brain regions that respond to SEMA, namely the nucleus of the solitary tract (NTS) – a key integration center for peripheral signals that help regulate feeding behavior. To test this, we sequenced RNA from the NTS of C57BL/6J mice, which lose significant weight on SEMA, and New Zealand Obese mice, which do not lose weight on SEMA. Identifying genetic differences between these strains will help us identify potential targets for future obesity drugs that work better across genetically diverse populations.