Arianna Kapotas
Pronouns: She/ Her/ Hers
Research Mentor(s): Rebecca Schill
Co-Presenter:
Research Mentor School/College/Department: Molecular & Integrative Physiology / Medicine
Presentation Date: April 20
Presentation Type: Poster
Session: Session 6 – 4:40pm – 5:30 pm
Room: League Ballroom
Authors: Arianna N. Kapotas, Jessica N. Maung, Rebecca L. Schill
Presenter: 25
Abstract
Familial partial lipodystrophy type 2 (FPLD2) is a condition that causes an abnormal distribution of adipose tissue throughout the body. FPLD2 is caused by mutations to the gene LMNA, which encodes for the protein lamin A/C. Though it is known that FPLD2 is caused by a mutation in LMNA, the mechanism of adipose tissue loss is unknown. Individuals with FPLD2 experience a sudden loss of adipose tissue around the time of puberty. To study FPLD2, we are using a mouse model with the LMNA gene knocked out of adipose tissue. Mice lacking the LMNA gene demonstrate most of the phenotypes seen in FPLD2. One hypothesis for the mechanism of fat loss in FPLD2 is enhanced lipolysis. To test this hypothesis, we are quantifying adipocyte size at different time points. By doing this, we hope to gain a greater understanding of what mechanisms are involved in the loss of adipose tissue in individuals with FPLD2. Additionally, we are performing metabolic studies using this model, including ITTs and GTTs, to better understand how adipose tissue loss contributes to metabolic dysfunction in FPLD2. Results from these studies will lead to a greater understanding of FPLD2 and may contribute to better treatment options for FPLD2 patients.
Biomedical Sciences, Interdisciplinary
