Madyson Woodburn
Molecular Biology Discipline, Natural Sciences Collegium, Eckerd College, St. Petersburg, FL
Dr. Whitney Bullock
Molecular Biology Discipline, Natural Sciences Collegium, Eckerd College, St. Petersburg, FL
Sarcopenia is an age-related gradual loss of skeletal muscle mass that results in muscle atrophy.1 Lean muscle mass has been displayed to significantly decrease in individuals with this disorder, and the progressive loss of muscle mass ultimately contributes to a higher fat mass distribution throughout the body. The pathogenic mechanisms that contribute to the gradual decrease in muscle fibers still remain unknown.1,2 Ghrelin has been shown to be a therapeutic treatment solution for individuals with sarcopenia, as it has been shown to improve muscle wasting by measuring increases in muscular strength and lean body mass.3 Although ghrelin has appeared to have a positive impact on muscle-to-fat differentiation in individuals with sarcopenia, the mechanical properties of how it improves their muscular ratio are still unclear. This study aimed to examine the pathogenic effects that ghrelin has on muscle-to-fat differentiation within mesenchymal progenitor cells (MPCs). Differentiation of MPCs with myogenic or adipogenic selective media drove characteristic differentiation into myocyte-like or adipocyte-like cells, respectively. Myogenic cells became elongated and displayed fibrous characteristics indicative of myogenic differentiation. Conversely, cells exposed to adipogenic media developed increases in cytoplasmic lipid droplets and a rounded appearance, indicative of adipogenic differentiation. Future research entails confirmation of differentiation with protein and gene expression, plus deletion of ghrelin expression. In this study, we were able to gain insight into the pathogenic mechanisms involved in the muscle-to-fat differentiation of MPCs, which can ultimately contribute to learning more about the pathogenic mechanisms involved with individuals with sarcopenia.
For more information: mewoodbu@eckerd.edu