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.

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.

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.

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.

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.

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.

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.

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.

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.

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.