Current and Past Colorado NORC Pilot Awardees
Funding Year 2024
Jill Chang, MD
Dates of Funding: 2024-2026
“Metabolic reprogramming of oligodendrocytes in intrauterine growth restriction”
Infants born following intrauterine growth restriction (IUGR) are recognized to be at risk for the development of cerebral palsy (CP). White matter injury (WMI), the histopathological correlate to CP, has been well documented in human and animal studies of IUGR. Existing literature suggests that impaired oligodendrocyte (OL) differentiation may be responsible for the WMI seen in IUGR. This project will evaluate a potential bioenergetic mechanism for impaired OL differentiation in PI-IUGR with the central hypothesis that PI-IUGR leads to metabolic reprogramming of OPCs, which results in long term impairments in differentiation and myelination. The experiments proposed in this application will evaluate this hypothesis using Agilent Seahorse technology to characterize substrate dependency, capacity, and flexibility of OPCs exposed to PI-IUGR.
Tyler Cook, PhD
Years of Funding 2024-2026
“Mechanisms of portal glucose sensing”
I am a postdoctoral fellow in the Pediatrics Department, Nutrition Division. My research goal is to understand how nutrient signals are detected and integrated into the brain to control energy balance and glucose homeostasis. I am currently funded through a T32 from the Pediatrics Nutrition Division, and I have also received a NIH/NIDDK F32 Fellowship investigating neuronal mechanisms associated with postbariatric hypoglycemia.
For my Colorado NORC pilot award, I am investigating how peripheral sensory neurons detect changes in blood glucose to maintain glucose homeostasis. Sensory neurons innervate the gastrointestinal tract and rapidly transmit nutrient signals to the brain before the nutrients even hit systemic circulation. In obesity, these sensory mechanisms likely become overwhelmed and contribute to the dysregulation of energy balance and glycemia. By understanding the mechanisms of neuronal glucose sensing, and how obesity disrupts these processes, I hope to identify new therapeutic targets for metabolic disease.
Stephanie Gilley, MD, PhD
Years of Funding: 2024-2026
“Solving a big problem for tiny babies: Digital body composition for infants”
I am an assistant professor in the Section of Nutrition, Department of Pediatrics. My research centers on understanding the earliest origins of health and disease and how we should feed infants and toddlers based on their intrauterine exposures. Body composition is an essential outcome measure to fully understand the impact of early life nutrition interventions. Despite the importance of body composition, most large research studies are limited to simple anthropometric measurements such as weight, height and BMI, limiting their impact. Major limitations to assessing body composition longitudinally in children include cost, acquisition time, radiation exposure, and/or requirement for trained personnel. Our project aims to develop a novel method for assessing body composition in infants using digital photography. Ready access to body composition will improve infant nutritional and growth monitoring and, in turn, directly impact patient outcomes.
Emily Hill, PhD, RDN
Years of Funding: 2024-2026
“Defining impact of changes in dietary intake patterns using -omics assessments within behavioral weight loss interventions”
I am a Research Instructor/Fellow and Registered Dietitian Nutritionist (RDN) with extensive training in nutrition and clinical and translational research. My research objective is to develop an independent research program that: 1) rigorously develops and tests interventions to improve adherence to evidence-based guidelines for lifestyle behaviors and 2) incorporates -omics approaches to predict and evaluate response to intervention. My current work is funded through a National Cancer Institute K99/R00 award (K99 CA287061) and builds upon a recently completed proof-of-concept trial that I implemented at the University of Colorado Cancer Center. Through these efforts, I am developing a survivorship nutrition intervention, called BfedBwell, to be integrated within the existing BfitBwell cancer exercise program. The goal is to use the Multiphase Optimization STrategy (MOST) framework to create a comprehensive program that will help adults with a history of cancer and overweight/obesity to improve diet and physical activity patterns. I am leading a 2^3 factorial trial to test three different program components alongside a core education curriculum. My Colorado NORC Pilot Award will allow me to leverage this clinical trial to collect additional biological samples and associated data necessary to evaluate the intervention through the incorporation of targeted and untargeted -omics approaches. Using these approaches, I will be able to assess change in exposure to a high-quality dietary pattern and explore associations with cardiometabolic health via integrated network analysis. Future work will include a fully-powered R01 optimization trial of the BfedBwell program and adaptation for dissemination to other settings and populations.
Matthew Olm, PhD
Years of Funding 2024-2026
"Quantifying the impact of first foods on the infant gut microbiota and immune health"
I am an Assistant Professor at the University of Colorado, Boulder. In this study, I aim to investigate how the first foods infants consume influence the development of their gut microbiome and its interaction with the immune system. Early-life diet plays a crucial role in shaping long-term health outcomes, including risks for obesity and autoimmune diseases. However, there is still a lack of evidence-based guidelines for optimal first foods. To address this, I will use metagenomic immunoglobulin sequencing (MIg-Seq) to study how different diets—specifically meat, dairy, plant-based, and control diets—affect IgA (immunoglobulin A) binding in the gut microbiota. My research will focus on how diet modulates IgA specificity and production, which in turn influences the colonization of beneficial microbes. Through this study, I hope to uncover dietary factors that promote healthy immune development and microbiome composition, with the ultimate goal of informing dietary recommendations for infants. This project builds on my expertise in microbiome research and has the potential to expand to additional study sites and populations.
Funding Year 2023
Andrew Libby PhD
Post-Doctoral Fellow
- Endocrinology (SOM)
Email Address:andrew.libby@ucdenver.edu
Primary Phone:3037246878
Mailing Address:
- CU Anschutz
Research I North
12800 East 19th Avenue
Rm 5402L
Aurora, CO 80045
Dates of funding: 2021-2023
Loss of ovarian function greatly increases the risk of non-alcoholic fatty liver (NAFLD) in humans and rodents, and therapies available to treat this disorder are limited. In addition to other mechanisms that have been described, it’s likely that changes in adipose tissue in the postmenopausal state also contribute to NAFLD. Specifically, menopause and ovariectomy (OVX) favor the accumulation of pro-inflammatory bone marrow-derived adipocytes (BMDA) that may change the cellular composition of abdominal fat by enriching it with adipocytes that export harmful factors to the liver, and mechanisms that modulate BMDA infiltration are poorly understood. I hypothesize that limited calorie diets can restrict abdominal BMDA infiltration to improve NAFLD in rodents that undergo OVX, and I also propose that BMDA play a substantial direct role in mediating OVX-induced NAFLD development. To test this, 1) I will use weight maintenance and caloric restriction diets in mice that undergo OVX to determine if this strategy reduces BMDA infiltration and limits NAFLD progression, and 2) I will use genetic ablation of BMDA in OVX mice to test their direct contribution to NAFLD. Data obtained from these aims will provide novel insight into OVX-induced NAFLD and provide new therapeutic targets to treat this disorder.
Funding Year 2022
Andrew Libby PhD
Post-Doctoral Fellow
- Endocrinology (SOM)
Email Address:andrew.libby@ucdenver.edu
Primary Phone:3037246878
Mailing Address:
- CU Anschutz
Research I North
12800 East 19th Avenue
Rm 5402L
Aurora, CO 80045
Dates of funding: 2021-2023
Loss of ovarian function greatly increases the risk of non-alcoholic fatty liver (NAFLD) in humans and rodents, and therapies available to treat this disorder are limited. In addition to other mechanisms that have been described, it’s likely that changes in adipose tissue in the postmenopausal state also contribute to NAFLD. Specifically, menopause and ovariectomy (OVX) favor the accumulation of pro-inflammatory bone marrow-derived adipocytes (BMDA) that may change the cellular composition of abdominal fat by enriching it with adipocytes that export harmful factors to the liver, and mechanisms that modulate BMDA infiltration are poorly understood. I hypothesize that limited calorie diets can restrict abdominal BMDA infiltration to improve NAFLD in rodents that undergo OVX, and I also propose that BMDA play a substantial direct role in mediating OVX-induced NAFLD development. To test this, 1) I will use weight maintenance and caloric restriction diets in mice that undergo OVX to determine if this strategy reduces BMDA infiltration and limits NAFLD progression, and 2) I will use genetic ablation of BMDA in OVX mice to test their direct contribution to NAFLD. Data obtained from these aims will provide novel insight into OVX-induced NAFLD and provide new therapeutic targets to treat this disorder.
Funding Year 2021
Andrew Libby PhD
Post-Doctoral Fellow
- Endocrinology (SOM)
Email Address:andrew.libby@ucdenver.edu
Primary Phone:3037246878
Mailing Address:
- CU Anschutz
Research I North
12800 East 19th Avenue
Rm 5402L
Aurora, CO 80045
Dates of funding: 2021-2023
Loss of ovarian function greatly increases the risk of non-alcoholic fatty liver (NAFLD) in humans and rodents, and therapies available to treat this disorder are limited. In addition to other mechanisms that have been described, it’s likely that changes in adipose tissue in the postmenopausal state also contribute to NAFLD. Specifically, menopause and ovariectomy (OVX) favor the accumulation of pro-inflammatory bone marrow-derived adipocytes (BMDA) that may change the cellular composition of abdominal fat by enriching it with adipocytes that export harmful factors to the liver, and mechanisms that modulate BMDA infiltration are poorly understood. I hypothesize that limited calorie diets can restrict abdominal BMDA infiltration to improve NAFLD in rodents that undergo OVX, and I also propose that BMDA play a substantial direct role in mediating OVX-induced NAFLD development. To test this, 1) I will use weight maintenance and caloric restriction diets in mice that undergo OVX to determine if this strategy reduces BMDA infiltration and limits NAFLD progression, and 2) I will use genetic ablation of BMDA in OVX mice to test their direct contribution to NAFLD. Data obtained from these aims will provide novel insight into OVX-induced NAFLD and provide new therapeutic targets to treat this disorder.
Funding Year 2020
Andrew Libby PhD
Post-Doctoral Fellow
- Endocrinology (SOM)
Email Address:andrew.libby@ucdenver.edu
Primary Phone:3037246878
Mailing Address:
- CU Anschutz
Research I North
12800 East 19th Avenue
Rm 5402L
Aurora, CO 80045
Dates of funding: 2021-2023
Loss of ovarian function greatly increases the risk of non-alcoholic fatty liver (NAFLD) in humans and rodents, and therapies available to treat this disorder are limited. In addition to other mechanisms that have been described, it’s likely that changes in adipose tissue in the postmenopausal state also contribute to NAFLD. Specifically, menopause and ovariectomy (OVX) favor the accumulation of pro-inflammatory bone marrow-derived adipocytes (BMDA) that may change the cellular composition of abdominal fat by enriching it with adipocytes that export harmful factors to the liver, and mechanisms that modulate BMDA infiltration are poorly understood. I hypothesize that limited calorie diets can restrict abdominal BMDA infiltration to improve NAFLD in rodents that undergo OVX, and I also propose that BMDA play a substantial direct role in mediating OVX-induced NAFLD development. To test this, 1) I will use weight maintenance and caloric restriction diets in mice that undergo OVX to determine if this strategy reduces BMDA infiltration and limits NAFLD progression, and 2) I will use genetic ablation of BMDA in OVX mice to test their direct contribution to NAFLD. Data obtained from these aims will provide novel insight into OVX-induced NAFLD and provide new therapeutic targets to treat this disorder.
Funding Year 2019
Andrew Libby PhD
Post-Doctoral Fellow
- Endocrinology (SOM)
Email Address:andrew.libby@ucdenver.edu
Primary Phone:3037246878
Mailing Address:
- CU Anschutz
Research I North
12800 East 19th Avenue
Rm 5402L
Aurora, CO 80045
Dates of funding: 2021-2023
Loss of ovarian function greatly increases the risk of non-alcoholic fatty liver (NAFLD) in humans and rodents, and therapies available to treat this disorder are limited. In addition to other mechanisms that have been described, it’s likely that changes in adipose tissue in the postmenopausal state also contribute to NAFLD. Specifically, menopause and ovariectomy (OVX) favor the accumulation of pro-inflammatory bone marrow-derived adipocytes (BMDA) that may change the cellular composition of abdominal fat by enriching it with adipocytes that export harmful factors to the liver, and mechanisms that modulate BMDA infiltration are poorly understood. I hypothesize that limited calorie diets can restrict abdominal BMDA infiltration to improve NAFLD in rodents that undergo OVX, and I also propose that BMDA play a substantial direct role in mediating OVX-induced NAFLD development. To test this, 1) I will use weight maintenance and caloric restriction diets in mice that undergo OVX to determine if this strategy reduces BMDA infiltration and limits NAFLD progression, and 2) I will use genetic ablation of BMDA in OVX mice to test their direct contribution to NAFLD. Data obtained from these aims will provide novel insight into OVX-induced NAFLD and provide new therapeutic targets to treat this disorder.
Funding Year 2018
Andrew Libby PhD
Post-Doctoral Fellow
- Endocrinology (SOM)
Email Address:andrew.libby@ucdenver.edu
Primary Phone:3037246878
Mailing Address:
- CU Anschutz
Research I North
12800 East 19th Avenue
Rm 5402L
Aurora, CO 80045
Dates of funding: 2021-2023
Loss of ovarian function greatly increases the risk of non-alcoholic fatty liver (NAFLD) in humans and rodents, and therapies available to treat this disorder are limited. In addition to other mechanisms that have been described, it’s likely that changes in adipose tissue in the postmenopausal state also contribute to NAFLD. Specifically, menopause and ovariectomy (OVX) favor the accumulation of pro-inflammatory bone marrow-derived adipocytes (BMDA) that may change the cellular composition of abdominal fat by enriching it with adipocytes that export harmful factors to the liver, and mechanisms that modulate BMDA infiltration are poorly understood. I hypothesize that limited calorie diets can restrict abdominal BMDA infiltration to improve NAFLD in rodents that undergo OVX, and I also propose that BMDA play a substantial direct role in mediating OVX-induced NAFLD development. To test this, 1) I will use weight maintenance and caloric restriction diets in mice that undergo OVX to determine if this strategy reduces BMDA infiltration and limits NAFLD progression, and 2) I will use genetic ablation of BMDA in OVX mice to test their direct contribution to NAFLD. Data obtained from these aims will provide novel insight into OVX-induced NAFLD and provide new therapeutic targets to treat this disorder.
Funding Year 2017
Andrew Libby PhD
Post-Doctoral Fellow
- Endocrinology (SOM)
Email Address:andrew.libby@ucdenver.edu
Primary Phone:3037246878
Mailing Address:
- CU Anschutz
Research I North
12800 East 19th Avenue
Rm 5402L
Aurora, CO 80045
Dates of funding: 2021-2023
Loss of ovarian function greatly increases the risk of non-alcoholic fatty liver (NAFLD) in humans and rodents, and therapies available to treat this disorder are limited. In addition to other mechanisms that have been described, it’s likely that changes in adipose tissue in the postmenopausal state also contribute to NAFLD. Specifically, menopause and ovariectomy (OVX) favor the accumulation of pro-inflammatory bone marrow-derived adipocytes (BMDA) that may change the cellular composition of abdominal fat by enriching it with adipocytes that export harmful factors to the liver, and mechanisms that modulate BMDA infiltration are poorly understood. I hypothesize that limited calorie diets can restrict abdominal BMDA infiltration to improve NAFLD in rodents that undergo OVX, and I also propose that BMDA play a substantial direct role in mediating OVX-induced NAFLD development. To test this, 1) I will use weight maintenance and caloric restriction diets in mice that undergo OVX to determine if this strategy reduces BMDA infiltration and limits NAFLD progression, and 2) I will use genetic ablation of BMDA in OVX mice to test their direct contribution to NAFLD. Data obtained from these aims will provide novel insight into OVX-induced NAFLD and provide new therapeutic targets to treat this disorder.
Funding Year 2016
Funding Year 2015
Andrew Libby PhD
Post-Doctoral Fellow
- Endocrinology (SOM)
Email Address:andrew.libby@ucdenver.edu
Primary Phone:3037246878
Mailing Address:
- CU Anschutz
Research I North
12800 East 19th Avenue
Rm 5402L
Aurora, CO 80045
Dates of funding: 2021-2023
Loss of ovarian function greatly increases the risk of non-alcoholic fatty liver (NAFLD) in humans and rodents, and therapies available to treat this disorder are limited. In addition to other mechanisms that have been described, it’s likely that changes in adipose tissue in the postmenopausal state also contribute to NAFLD. Specifically, menopause and ovariectomy (OVX) favor the accumulation of pro-inflammatory bone marrow-derived adipocytes (BMDA) that may change the cellular composition of abdominal fat by enriching it with adipocytes that export harmful factors to the liver, and mechanisms that modulate BMDA infiltration are poorly understood. I hypothesize that limited calorie diets can restrict abdominal BMDA infiltration to improve NAFLD in rodents that undergo OVX, and I also propose that BMDA play a substantial direct role in mediating OVX-induced NAFLD development. To test this, 1) I will use weight maintenance and caloric restriction diets in mice that undergo OVX to determine if this strategy reduces BMDA infiltration and limits NAFLD progression, and 2) I will use genetic ablation of BMDA in OVX mice to test their direct contribution to NAFLD. Data obtained from these aims will provide novel insight into OVX-induced NAFLD and provide new therapeutic targets to treat this disorder.
Funding Year 2014
Andrew Libby PhD
Post-Doctoral Fellow
- Endocrinology (SOM)
Email Address:andrew.libby@ucdenver.edu
Primary Phone:3037246878
Mailing Address:
- CU Anschutz
Research I North
12800 East 19th Avenue
Rm 5402L
Aurora, CO 80045
Dates of funding: 2021-2023
Loss of ovarian function greatly increases the risk of non-alcoholic fatty liver (NAFLD) in humans and rodents, and therapies available to treat this disorder are limited. In addition to other mechanisms that have been described, it’s likely that changes in adipose tissue in the postmenopausal state also contribute to NAFLD. Specifically, menopause and ovariectomy (OVX) favor the accumulation of pro-inflammatory bone marrow-derived adipocytes (BMDA) that may change the cellular composition of abdominal fat by enriching it with adipocytes that export harmful factors to the liver, and mechanisms that modulate BMDA infiltration are poorly understood. I hypothesize that limited calorie diets can restrict abdominal BMDA infiltration to improve NAFLD in rodents that undergo OVX, and I also propose that BMDA play a substantial direct role in mediating OVX-induced NAFLD development. To test this, 1) I will use weight maintenance and caloric restriction diets in mice that undergo OVX to determine if this strategy reduces BMDA infiltration and limits NAFLD progression, and 2) I will use genetic ablation of BMDA in OVX mice to test their direct contribution to NAFLD. Data obtained from these aims will provide novel insight into OVX-induced NAFLD and provide new therapeutic targets to treat this disorder.