Current and Past Colorado NORC Pilot Awardees

Funding Year 2024

Funding Year 2023

libby

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

libby

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

libby

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

libby

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

libby

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

libby

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

libby

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

libby

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

libby

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.

Colorado Nutrition Obesity Research Center (NORC)

CU Anschutz Health and Wellness Center

12348 East Montview Boulevard

Aurora, CO 80045


norc@cuanschutz.edu

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