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Chukwuebuka Okorie

Poster #071, Charles R. Drew University of Medicine and Science

Activation of Ectopic Olfactory Receptors in Skeletal Muscle in an In Vitro Model of Exercise

Mentor: Susana Cavallero, PhD

Some individuals are unable to engage in physical exercise due to structural barriers, physical disabilities or a lack of time or money to dedicate towards exercise-related equipment. To simulate the physiological benefits of a workout for these individuals, azelaic acid (AzA) has the potential to be used in exercise-replacement treatments. The cycle of contraction and relaxation in skeletal muscle during exercise induces biochemical processes and the release of myokines into the bloodstream. Olfactory receptor 544 (Olfr544), ectopically expressed outside of nasal tissue, triggers skeletal muscle to stimulate beneficial metabolic processes when ligand AzA molecules bind to Olfr544, activating the downstream PKA-CREB-PGC-1α signaling pathway. Both processes result in mitochondrial biogenesis causing the muscle to increase glucose uptake. This study aims to determine if administration of AzA is as or more effective than electrical pulse stimulation (EPS) at expressing Olfr544 in skeletal muscle. Mouse skeletal C2C12 cells were cultured and differentiated to myotubes in DMEM with 2% horse serum. Myotubes remained unstimulated or received EPS using an IonOptix C-Pace machine for one hour, which delivered regular electrical currents at 20V in 0.2 ms durations, in the presence or absence of 50μM AzA. Mitochondrial biogenesis was measured through Mitotracker staining. Olfr544 expression was assessed by western Blot and immunofluorescence. In summary, EPS allows us to create an “exercise in a dish” model to study exercise using cultured cells. Our preliminary results suggest that ectopic ORs could be involved in the molecular responses to exercise. In the future, similar studies could continue to explore the potential of AzA by adjusting AzA concentration levels and applying this study’s methodology to in vivo models.