2018 Abstracts

Joseph Millar, Utah Valley University

Anastasiia Matkovska; Austin Bettridge; Blake Allred; Jeff Keller, Utah Valley University

Jackson Podis, Westminster College In the Guna Yala archipelago, PanamÌÁ, the removal of coral species for construction of coral walls has been a common practice for the Guna Yala indigenous group. This practice has the potential to drastically alter the community structure of offshore reefs. This study analyzed three reefs offshore of islands with varying coral wall volumes to quantify macroalgae and scleractinian coral cover, diversity of scleractinian coral species, and correlation between macroalgae and scleractinian coral cover. All three study sites exhibited significant differences in scleractinian coral coverage; a significant negative correlation was shown between scleractinian coral cover and macroalgal cover, and the site with the largest coral wall volume showed the lowest rates of coral species commonly used for mining. These results are telling of the potential effects coral mining can have on coral reefs in the Guna Yala archipelago, and aim to inform the development of marine resource management plans in the future.

Thomas Shober; Jaxon Roller; Ashley Kennedy, University of Utah

Joseph Rich, Brigham Young University

Chase Omana, University of Utah

Konstantinos Karpos; Koren Roach, University of Utah

Kyle Hakes; Heather Erickson, Brigham Young University

Jessica Mancuso, Southern Utah University

Eric Gibson, Weber State University

Matthew Thompson, Utah State University

Jhana Aristondo, Utah Valley University

Whittni Ananin, Southern Utah University

Christine Rumsey; Andrew Piskadlo; Adele Reynolds; Ryan Rowland; Shu Yang; Bill Johnson; Anna Robert; Gaurav Pandey, Westminster

Madalyn Johnson; Megan Anderson, Utah Valley University

Allison White, Dixie State University

Katherine Safsten, Brigham Young University

Kathleen Fotheringham, Southern Utah University

Sydnee Higginson, Brigham Young University

Keanna Graff, Dixie State University

Maggie Marchant, Brigham Young University

Dakota Halley; Stephanie Johnstone; Andrea Deever; Cassidie Medina; Kimberly Child, Dixie State University

Mark Albrecht; Kristin Wilson-Grimes; Sennai Habtes, Southern Utah University

Rachel Fuller, Brigham Young University

Jaimi Butler; Ashley Kijowski; Claire Prasad, Westminster College

Diabetes affects over 30 million Americans and 185,000 Utahn’s. Type 1 and Type 2 diabetes are characterized by decreased functional β-cell mass and insulin production. Diabetes also results in increased circulating glucose and fatty acid levels, which damage and destroy β-cells over time. Our study will shed further light on the effects of palmitate, the most commonly made fatty acid in the liver, on hyperlipidemia. In this study we test the specific effects of chronic palmitate exposure on various cell lines acclimated to 0.15 mM, 0.3 mM, and 0.5 mM concentrations of palmitate. We demonstrate the effects of progressive long-term exposure to palmitate on β-cell proliferation and resistance to apoptosis. We demonstrate mechanistic changes that result in the observed phenotypes. Our goal in this study is to explore how β-cells adapt to exposure to hyperlipidemia, and to define interventions to protect β-cells from the harmful effects of hyperlipidemia.

Jacob Delano; Nicholas Brian, Utah Valley University

Ashley Wiltsie, University of Utah

Aaron Leifer, Jasmine Banner, Collin Christensen, Trevor Lloyd, Kenneth Call, Brigham Young University Diabetes Mellitus has become a worldwide epidemic affecting over 400 million people. Both type 1 and type 2 diabetes result from the body’s inability to produce or respond to insulin in order to regulate blood sugar. In both cases, the insulin secreting ë_-cells in the pancreatic Islets of Langerhans have become endangered and in many cases non-functional. The function of these ë_-cells is defined by their ability to multiply and maintain a steady number, to defend against induced cell death and ultimately to secrete insulin. Since ë_-cell production reaches its peak during fetal development, this would suggest that diabetics have an inactive pathway to produce functional ë_-cells. However, recent studies have identified key transcription factors that aid pancreatic progenitors in becoming functional ë_-cells. Pdx1 is a transcription factor that is active throughout the ë_-cell pathway and found in mature ë_-cells. Research has identified Pdx1 as a key component in helping both ë±-cells and ë_-cells proliferate and even in reprogramming ë±-cells to become functional ë_-cells. Additionally, Pdx1 has been identified to help ë_-cells effectively secrete insulin. We present data demonstrating the effect of Pdx1 adenoviral over-expression on three independent markers of functional ë_-cell mass: 1) cell proliferation, 2) cell survival, and 3) insulin content and secretion. Defining the effect of Pdx1 on each of these parameters will provide further data to explore therapeutic interventions for diabetic patients.

Karaleen Anderson; Mariel Hatch, Utah Valley University

Parker Booren, Nathanael Jensen, Talon Aitken, Samuel Grover, Jackie Crabree, Brigham Young University Diabetes continues to grow at a rapid rate, affecting the lives of both young and old. Both Type 1 and Type 2 diabetes lead to eventual ë_ cell depletion (and subsequent decrease in insulin secretion). This can be treated through ë_ cell transplantation from the pancreata of cadavers. Currently, collecting sufficient ë_ cells for one diabetic patient requires pancreata from multiple cadavers. If proliferation can be induced in a donor’s aged ë_ cells, transplantation would become more effective as one donor now becomes sufficient to serve one or two patients. Nkx6.1 is a transcription factor that increases insulin secretion and induces proliferation of young rat ë_ cells (5 weeks) through the upregulation of its target genes: VGF, Nr4a1 and Nr4a3. Aged rat ë_ cells (5+ months) fail to proliferate after overexpression of Nkx6.1. We have also shown that upregulation of Nkx6.1’s target genes is disrupted in these aged ë_ cells. This may be due to changes in expression of a binding partner necessary for Nkx6.1’s upregulation of these target genes or to changes in Nkx6.1 posttranslational modifications that impede binding partner interactions in aged ë_ cells. We present data from co-immunoprecipitation and mass spectrometry experiments that reveal the presence or absence of Nkx6.1’s binding partner in young and aged ë_ cells. Furthermore, we present mass spectrometry results of Nkx6.1 posttranslational modification from young and old ë_ cells. This data will increase understanding on the ability of Nkx6.1 to upregulate its target genes in an aged ë_ cell.

Colton Smith, Dixie State University

Kayleigh Ingersoll, Brigham Young University

Nayla Rhein, Southern Utah University

Trevor Lloyd; Mason Poffenbarger; Austin Ricks; Andrew Barlow; Zoey Fishburn, Brigham Young University

Lydia Morley, University of Utah

Alyson DeNittis, Utah Valley University

Michael Lange; Don Rodriguez; Elijah Bingham, Brigham Young University

Agueda Rodriguez; Michael Hope, Southern Utah University

Karaleen Anderson; Mariel Hatch; Caeleb Harris; Karina Bravo; Rawly Lyle; Tyson Hill, Utah Valley University

Nadja Redd; Gloria Slattum; Jody Rosenblatt; Franco Jin, University of Utah

Mark Albrecht; Brock Orme; Mary Jo Tufte, Southern Utah University

Grace Hoffmann; Monika Lakk, University of Utah

Aaron Wallace; Brad Hauck; Michelle White; Michele Hansen, University of Utah

Mariah Clayson; Maverik Shumway; Brian Anderson, Southern Utah University

Hal Jones; Dan Schindler; Brynne Anderson; Mary Rosbach; Chandler Warr, Brigham Young University

Erin Kinnally; John Capitanio; Elizabeth Wood; Angus Bennion; Ryno Kruger; Christina Barr; Stephen Lindell; Stephen Suomi, Brigham Young University

Jacob Shaner, Brigham Young University

Kirk Harter; Spencer Drennan; Liza Jarman; Weon Kim; Gregory Boatwright, Brigham Young University

Courtney Smith, Brigham Young University