Life Sciences

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.

2018 Abstracts

Rearing Ephemeroptera in the Lab: Parthenogenesis and Transcriptome Data In the Mayflies

January 01, 2018 12:00 AM

Jacob Delano; Nicholas Brian, Utah Valley University

2018 Abstracts

The effect of the loss of nonsense-mediated mRNA decay on naturally occurring variants

January 01, 2018 12:00 AM

Ashley Wiltsie, University of Utah

2018 Abstracts

Does Pdx1 Enhance Functional ë_-cell Mass?

January 01, 2018 12:00 AM

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.

2018 Abstracts

Biofilm induction in mucormycosis-causing fungi and the synergistic antifungal activity of amphotericin B and thyme oil

January 01, 2018 12:00 AM

Karaleen Anderson; Mariel Hatch, Utah Valley University

2018 Abstracts

MafA’s Ability to Enhance ë_-cell Function

January 01, 2018 12:00 AM

Aaron Leifer, Jasmine Banner, Collin Christensen, Trevor Lloyd, Kenneth Call, Brigham Young University Approximately 9.4 percent of the United States is affected by type 1 or type 2 diabetes. Diabetes results from the body’s inability to maintain healthy blood glucose levels due to the loss of pancreatic ë_-cells (insulin secreting cells) or from the body’s insulin sensitive cells becoming insulin resistant. Both type 1 and type 2 diabetes results in a loss of functional ë_-cells. The current treatments for diabetes are insulin injections or transplants, many times requiring up to three donors per transplant. Neither option is an optimal cure: insulin injections do not cure the disease, and transplants are not available to the majority of people. We propose that being able to replicate ë_-cells in-vivo would allow us to provide a cure to diabetes. ë_-cells stop reproducing (proliferating) soon after birth except in a few occasions such as obesity and pregnancy, leading us to believe that there are key gene(s) that induce cell proliferation when activated. Finding these gene(s) would present a viable cure, being able to grow ë_-cells in-vivo for transplantation or even injection. The gene MafA is present in mature ë_-cells and previous research has revealed its vital role in the pancreas. MafA is turned on around embryonic day 15.5 and steadily increases expression up until the cell becomes a mature ë_-cell. The time period when MafA is turned on corresponds with when a ë_-cell is proliferating and developing leading us to believe that MafA is crucial to finding a cure. Here we show the effect of MafA overexpression on INS1 832/13 ë_-cell proliferation, survival, and insulin secretion.

2018 Abstracts

Barriers to the proliferation of aged ë_ cells through overexpression of Nkx6.1

January 01, 2018 12:00 AM

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.

2018 Abstracts