FOEDRC announces new pilot grant recipients

The Fraternal Order of Eagles Diabetes Research Center released the following announcement today.

The Fraternal Order of Eagles Diabetes Research Center at The University of Iowa, Carver College of Medicine, is pleased to announce the results of its ninth round of pilot and feasibility research grants. These grant awards fund innovative pilot projects by early career investigators who are entering the diabetes research field, or established investigators with innovative ideas that focus their research program in a new direction that addresses important questions in diabetes research. The goal of the program is to generate data that will enable awardees to compete for peer-reviewed national funding for projects that show exceptional promise. These pilot project research grants are supported by gifts from the Fraternal Order of Eagles, which now endow this grant program. This year we supported two types of applications. Catalyst awards fund pilot projects for up to two years as in prior years. New this year, were seed grants, which are small awards designed to support specific experiments that are required to provide critical preliminary data that would enable investigators to submit or re-submit grant proposals in the relative near- term. A total of 29 researchers from across the UI campus submitted meritorious proposals that underwent a comprehensive two-stage review.  The review panel had a challenging time to identify proposals for funding from such a competitive field. Two applicants were selected to receive a catalyst award grant of $50,000 to support their research proposal, with the possibility for a second year of funding, for a total of $100,000 over a two-year period. Three applicants were selected to receive a seed award grant of $6,500 to support critical experiments.

Congratulations to all of our 2019-2020 FOEDRC Pilot & Feasibility Grant Award Recipients!

AtasoyDeniz Atasoy, PhD
Assistant Professor
Department of Neuroscience and Pharmacology

Project Title: “Identifying the defective feeding pathways in hypoglycemia unawareness”
$50,000

Identify and validate hypoglycemic feeding pathways. Our project is based on preliminary results showing that a specialized neuron population in the brain, named AgRP-neurons, is required for hypoglycemic feeding. However, the pathways that activate AgRP neurons are not known. Therefore, we will first identify these pathways and then test whether they respond to hypoglycemia. Finally, we will test whether these pathways are required for hypoglycemic appetite upregulation. Upon successful completion, our results will lay the foundation for broader investigation into the disease mechanisms in these circuits.


CuiHuxing Cui, PhD
Assistant Professor
Department of Neuroscience and Pharmacology

Project Title: “Fine-mapping of pancreatic vagal circuit for systemic glucose homeostasis: the role of melanocortin signaling”
$50,000

Obesity and diabetes are serious chronic metabolic diseases affecting over 40% of adults in the United States. While autonomic nervous system is critical for key physiological processes involved in metabolic homeostasis and is dysfunctional in obesity and diabetes, the functional neuronal circuits regulating the physiology of key metabolic organs are largely unknown. Using advanced neuroscience tools combined with innovative viral-mediated circuit mapping technique, this research proposal seeks to decipher complex vagal afferent-efferent circuits that influence pancreatic function and systemic glucose homeostasis. It is our hope that the results from proposed studies can provide novel mechanistic insight into the neural control of whole-body metabolic homeostasis.


incemM. Nedim N. Ince, MD
Clinical Assistant Professor
Department of Internal Medicine – Gastroenterology and Hepatology

Project Title: “Single Cell Analysis of Adipose Tissue Regulatory T Cells”
$6,500

We propose to assess the transcriptional profile of regulatory T cells (Tregs) in adipose tissue using single cell RNA-seq. Preliminary studies from our group indicate that abnormal cytokine signaling to Tregs leads to weight gain and adiposity in mice. Future studies—with knocking out cytokine signaling intermediates—can uncover novel Treg-associated molecular mechanisms, critical to homeostasis of adipose tissue.


sivitzWilliam I. Sivitz, MD
Emeritus Professor
Department of Internal Medicine – Endocrinology and Metabolism

Project Title: “13C labelled isotopomer analysis for assessment of flux through oxaloacetate”
$6,500

We recently reported a biphasic, increasing then decreasing, respiratory response to increments in [ADP] in complex II (succinate)-energized mitochondria. In collaboration with Dr. Liping Yu, we developed an NMR method enabling specific and sensitive assessment of mitochondrial oxaloacetate (OAA) concentrations and used this method to show that the downturn in respiration was due to malate-derived OAA inhibition of succinate dehydrogenase (SDH). The ADP effect could be mimicked by perturbation of membrane potential by chemical uncoupling; suggesting that reduction in potential was the initiating or primary factor in the biphasic respiratory response. We then examined the role of OAA in brown adipose tissue (BAT) mitochondrial wherein membrane potentially is intrinsically low due to uncoupling protein 1 (UCP1). We showed that the UCP1-mediated decrease in membrane potential in succinate-energized mitochondria was accompanied by OAA inhibition of SDH and that inhibition of UCP1 decreased OAA and increased respiration. The current project will use MS- and NMR-based metabolomic measurements to assess OAA inhibition of SDH in intact cells and to determine the origin of OAA in cellular systems.


Vikram~AjitAjit Vikram, PhD
Assistant Professor
Internal Medicine – Cardiovascular Medicine

Project Title: “Early-life dysbiosis reprograms metabolic disorders through circulating microRNA-122”
$6,500

The miR-122 is a liver-specific miR and targets several genes involved in insulin-receptor signaling. The hypothesis of miR-122’s involvement derives its motivation from its gut-microbiota dependent regulation, resistance to the circulating RNases, and deregulation in the metabolic disorders. A proof of concept experiment establishing a causal connection between early-life dysbiosis to the later-life risk of obesity/diabetes through c-miR-122 following dysbiosis is critical. In this study, we are focusing on whether the miR-122 inhibition can rescue later-life obesity/diabetes following early-life microbial dysbiosis.

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