The 2018 Fall Undergraduate Research Festival (FURF) hosted by the Iowa Center for Research by Undergraduates was held on November 14, 2018. The Iowa Center for Research promotes undergraduate involvement in research and creative projects at the University of Iowa. FURF showcases visual presentations focusing on research and creative work performed by undergraduates at the University of Iowa. The presenters work within 40 different departments and major in over 35 different disciplines, including sciences, arts, and humanities.
Michael Westphal and Pooja Patel, both members of Dr. Abel’s laboratory, mentored by Renata Pereira received awards from the festival. Westphal, majoring Human Physiology presented a talk titled, “OPA1 Deficiency in Brown Adipose Tissue Prevents Diet-Induced Obesity and Insulin Resistance in Mice”. The presentation focused on Optic Atrophy 1 (OPA1), which is a mitochondrial protein that regulates mitochondrial dynamics and function. In mice, as well as our own bodies, there is brown fat and white fat. White fat is generally used for storage of excessive calories, while brown fat provides heat. They deleted the protein exclusively in brown fat in mice and analyzed the mitochondrial capacities, as well as the mice’s response to a high fat diet. The normal mice indicated diabetic symptoms and became obese, while the knockout mice did not gain weight and showed no diabetic symptoms. Westphal’s presentation received the Outstanding Poster Presentation award.
Patel, majoring in Biomedical Sciences presented a talk titled, “OPA1 Deficiency in BAT Results in Increased Cold Tolerance, Despite Impaired Mitochondrial Function in Female Mice”. Brown adipose tissue (BAT) becomes activated during cold to increase heat production, a process that requires adequate mitochondria function. They made mice that were deficient for OPA1, specifically in BAT and tested how they responded to short-term cold exposure. Female mice were found to be more tolerant of the cold temperatures when placed in short-term cold exposure. Mitochondria lacing the OPA1 protein had reduced function and looked structurally abnormal. Surprisingly, OPA1 deficient mice were more efficient in utilizing nutrients as fuel. Their white fat cells, which usually store energy in the form of fat, had an increased capacity to burn fat and glucose. The data concluded that removing the OPA1 protein from BAT leads to compensatory mechanisms, resulting in increased metabolism and resistance to cold. Patel’s presentation received the Distinguished Poster Presentation award.