Tamara Williams
Research Mentor: Brandon Buscher
Mentor Department: Pharmacology, Medicine
Author(s): Tamara Williams, Brandon Buscher, Monica Bame, Maddie Boleyn, Sonya Wolf
Session: Session 6 (3:00 PM – 3:50 PM)
Presentation Type: Poster 135
Abstract
Psoriasis is a chronic autoimmune disease that is caused by accumulation of immune cells and rapid division of keratinocytes, the primary cells in the skin epidermis, resulting in the development of persistent inflammation that presents as red, scaly plaques on the skin. Psoriasis has been linked to numerous systemic conditions such as metabolic syndrome, which predisposes an individual to develop diabetes, obesity, and cardiovascular disease. New research suggests that there are similar inflammatory pathways that may be contributing to both the development and pathogenesis of psoriasis and metabolic syndrome. In this study, the 7-day imiquimod induced murine model of psoriasis was used after 3 weeks on high fat diet (HFD) to investigate how changes in systemic metabolism contribute to the severity of psoriasis in a sex dependent manner. The severity of psoriasis was determined by back skin thickness measurements. We found that there was not a significant difference in psoriatic severity when comparing chow and HFD in both males and females. Additionally, a glucose tolerance test was performed to evaluate systemic metabolism. We found that there were sex dependent differences in glucose tolerance. Understanding the complex relationship between psoriasis and metabolic syndrome would allow for improved therapy development and allow for a deeper understanding of how patients with psoriasis are at an increased risk for metabolic disease.
