Dates of funding: 2018-2019
Ovulatory dysfunction is responsible for 25% of cases of subfertility and is frequently present in women with excessive body weight. Specifically, a high-fat intake causes excessive storage of lipid in non-adipose tissue, including the ovary, which can affect its physiological function and result in reproductive dysfunction in women. Recommended daily intake of fat is 20-30% of total calories, but most American women consume a diet containing at least 35%. Therefore, it is important to consider the impact of elevated dietary fat in ovarian dysfunction, especially as diets promoting high fat intake are becoming very popular, some resulting in a significant weight loss. There is theoretically a considerable population of women impacted by HFD-induced reproductive dysfunction of which the burden and mechanistic causes of action are undetermined. One potential reason why HFD causes an abnormal ovulatory function includes changes in genes critical to normal ovarian function. Endothelin-2 (Edn2), which is crucial in ovulation, was the most significantly altered gene upon exposure to HFD in my previous studies, regardless of obesity. Endothelin-2 (ET-2) is a recently identified protein that is secreted by ovarian granulosa cells and plays a critical role in ovulation and corpus luteum formation.The mechanisms regulating Edn2 expression in the ovary are not clear and in some cases controversial. Therefore my current research focuses on investigating mechanisms behind abnormal Edn2 expression in HFD exposure. Our central hypothesis is that HFD leads to diminished ovarian estrogen receptor (ER) signaling, with subsequent Edn2 downregulation and impaired ovulation. The knowledge that will be gained from the proposed experiments is critical to understanding the mechanisms behind HFD-induced ovulatory dysfunction. This new knowledge will help me uncover some important clues in previously unexplained ovulatory dysfunction and subfertility and design potential treatment strategies in women in the future.

Dates of funding: 2018-2019
Ovulatory dysfunction is responsible for 25% of cases of subfertility and is frequently present in women with excessive body weight. Specifically, a high-fat intake causes excessive storage of lipid in non-adipose tissue, including the ovary, which can affect its physiological function and result in reproductive dysfunction in women. Recommended daily intake of fat is 20-30% of total calories, but most American women consume a diet containing at least 35%. Therefore, it is important to consider the impact of elevated dietary fat in ovarian dysfunction, especially as diets promoting high fat intake are becoming very popular, some resulting in a significant weight loss. There is theoretically a considerable population of women impacted by HFD-induced reproductive dysfunction of which the burden and mechanistic causes of action are undetermined. One potential reason why HFD causes an abnormal ovulatory function includes changes in genes critical to normal ovarian function. Endothelin-2 (Edn2), which is crucial in ovulation, was the most significantly altered gene upon exposure to HFD in my previous studies, regardless of obesity. Endothelin-2 (ET-2) is a recently identified protein that is secreted by ovarian granulosa cells and plays a critical role in ovulation and corpus luteum formation.The mechanisms regulating Edn2 expression in the ovary are not clear and in some cases controversial. Therefore my current research focuses on investigating mechanisms behind abnormal Edn2 expression in HFD exposure. Our central hypothesis is that HFD leads to diminished ovarian estrogen receptor (ER) signaling, with subsequent Edn2 downregulation and impaired ovulation. The knowledge that will be gained from the proposed experiments is critical to understanding the mechanisms behind HFD-induced ovulatory dysfunction. This new knowledge will help me uncover some important clues in previously unexplained ovulatory dysfunction and subfertility and design potential treatment strategies in women in the future.

Dates of funding: 2018-2019
Ovulatory dysfunction is responsible for 25% of cases of subfertility and is frequently present in women with excessive body weight. Specifically, a high-fat intake causes excessive storage of lipid in non-adipose tissue, including the ovary, which can affect its physiological function and result in reproductive dysfunction in women. Recommended daily intake of fat is 20-30% of total calories, but most American women consume a diet containing at least 35%. Therefore, it is important to consider the impact of elevated dietary fat in ovarian dysfunction, especially as diets promoting high fat intake are becoming very popular, some resulting in a significant weight loss. There is theoretically a considerable population of women impacted by HFD-induced reproductive dysfunction of which the burden and mechanistic causes of action are undetermined. One potential reason why HFD causes an abnormal ovulatory function includes changes in genes critical to normal ovarian function. Endothelin-2 (Edn2), which is crucial in ovulation, was the most significantly altered gene upon exposure to HFD in my previous studies, regardless of obesity. Endothelin-2 (ET-2) is a recently identified protein that is secreted by ovarian granulosa cells and plays a critical role in ovulation and corpus luteum formation.The mechanisms regulating Edn2 expression in the ovary are not clear and in some cases controversial. Therefore my current research focuses on investigating mechanisms behind abnormal Edn2 expression in HFD exposure. Our central hypothesis is that HFD leads to diminished ovarian estrogen receptor (ER) signaling, with subsequent Edn2 downregulation and impaired ovulation. The knowledge that will be gained from the proposed experiments is critical to understanding the mechanisms behind HFD-induced ovulatory dysfunction. This new knowledge will help me uncover some important clues in previously unexplained ovulatory dysfunction and subfertility and design potential treatment strategies in women in the future.

Dates of funding: 2018-2019
Ovulatory dysfunction is responsible for 25% of cases of subfertility and is frequently present in women with excessive body weight. Specifically, a high-fat intake causes excessive storage of lipid in non-adipose tissue, including the ovary, which can affect its physiological function and result in reproductive dysfunction in women. Recommended daily intake of fat is 20-30% of total calories, but most American women consume a diet containing at least 35%. Therefore, it is important to consider the impact of elevated dietary fat in ovarian dysfunction, especially as diets promoting high fat intake are becoming very popular, some resulting in a significant weight loss. There is theoretically a considerable population of women impacted by HFD-induced reproductive dysfunction of which the burden and mechanistic causes of action are undetermined. One potential reason why HFD causes an abnormal ovulatory function includes changes in genes critical to normal ovarian function. Endothelin-2 (Edn2), which is crucial in ovulation, was the most significantly altered gene upon exposure to HFD in my previous studies, regardless of obesity. Endothelin-2 (ET-2) is a recently identified protein that is secreted by ovarian granulosa cells and plays a critical role in ovulation and corpus luteum formation.The mechanisms regulating Edn2 expression in the ovary are not clear and in some cases controversial. Therefore my current research focuses on investigating mechanisms behind abnormal Edn2 expression in HFD exposure. Our central hypothesis is that HFD leads to diminished ovarian estrogen receptor (ER) signaling, with subsequent Edn2 downregulation and impaired ovulation. The knowledge that will be gained from the proposed experiments is critical to understanding the mechanisms behind HFD-induced ovulatory dysfunction. This new knowledge will help me uncover some important clues in previously unexplained ovulatory dysfunction and subfertility and design potential treatment strategies in women in the future.

Dates of funding: 2018-2019
Ovulatory dysfunction is responsible for 25% of cases of subfertility and is frequently present in women with excessive body weight. Specifically, a high-fat intake causes excessive storage of lipid in non-adipose tissue, including the ovary, which can affect its physiological function and result in reproductive dysfunction in women. Recommended daily intake of fat is 20-30% of total calories, but most American women consume a diet containing at least 35%. Therefore, it is important to consider the impact of elevated dietary fat in ovarian dysfunction, especially as diets promoting high fat intake are becoming very popular, some resulting in a significant weight loss. There is theoretically a considerable population of women impacted by HFD-induced reproductive dysfunction of which the burden and mechanistic causes of action are undetermined. One potential reason why HFD causes an abnormal ovulatory function includes changes in genes critical to normal ovarian function. Endothelin-2 (Edn2), which is crucial in ovulation, was the most significantly altered gene upon exposure to HFD in my previous studies, regardless of obesity. Endothelin-2 (ET-2) is a recently identified protein that is secreted by ovarian granulosa cells and plays a critical role in ovulation and corpus luteum formation.The mechanisms regulating Edn2 expression in the ovary are not clear and in some cases controversial. Therefore my current research focuses on investigating mechanisms behind abnormal Edn2 expression in HFD exposure. Our central hypothesis is that HFD leads to diminished ovarian estrogen receptor (ER) signaling, with subsequent Edn2 downregulation and impaired ovulation. The knowledge that will be gained from the proposed experiments is critical to understanding the mechanisms behind HFD-induced ovulatory dysfunction. This new knowledge will help me uncover some important clues in previously unexplained ovulatory dysfunction and subfertility and design potential treatment strategies in women in the future.

Dates of funding: 2018-2019
Ovulatory dysfunction is responsible for 25% of cases of subfertility and is frequently present in women with excessive body weight. Specifically, a high-fat intake causes excessive storage of lipid in non-adipose tissue, including the ovary, which can affect its physiological function and result in reproductive dysfunction in women. Recommended daily intake of fat is 20-30% of total calories, but most American women consume a diet containing at least 35%. Therefore, it is important to consider the impact of elevated dietary fat in ovarian dysfunction, especially as diets promoting high fat intake are becoming very popular, some resulting in a significant weight loss. There is theoretically a considerable population of women impacted by HFD-induced reproductive dysfunction of which the burden and mechanistic causes of action are undetermined. One potential reason why HFD causes an abnormal ovulatory function includes changes in genes critical to normal ovarian function. Endothelin-2 (Edn2), which is crucial in ovulation, was the most significantly altered gene upon exposure to HFD in my previous studies, regardless of obesity. Endothelin-2 (ET-2) is a recently identified protein that is secreted by ovarian granulosa cells and plays a critical role in ovulation and corpus luteum formation.The mechanisms regulating Edn2 expression in the ovary are not clear and in some cases controversial. Therefore my current research focuses on investigating mechanisms behind abnormal Edn2 expression in HFD exposure. Our central hypothesis is that HFD leads to diminished ovarian estrogen receptor (ER) signaling, with subsequent Edn2 downregulation and impaired ovulation. The knowledge that will be gained from the proposed experiments is critical to understanding the mechanisms behind HFD-induced ovulatory dysfunction. This new knowledge will help me uncover some important clues in previously unexplained ovulatory dysfunction and subfertility and design potential treatment strategies in women in the future.

Dates of funding: 2018-2019
Ovulatory dysfunction is responsible for 25% of cases of subfertility and is frequently present in women with excessive body weight. Specifically, a high-fat intake causes excessive storage of lipid in non-adipose tissue, including the ovary, which can affect its physiological function and result in reproductive dysfunction in women. Recommended daily intake of fat is 20-30% of total calories, but most American women consume a diet containing at least 35%. Therefore, it is important to consider the impact of elevated dietary fat in ovarian dysfunction, especially as diets promoting high fat intake are becoming very popular, some resulting in a significant weight loss. There is theoretically a considerable population of women impacted by HFD-induced reproductive dysfunction of which the burden and mechanistic causes of action are undetermined. One potential reason why HFD causes an abnormal ovulatory function includes changes in genes critical to normal ovarian function. Endothelin-2 (Edn2), which is crucial in ovulation, was the most significantly altered gene upon exposure to HFD in my previous studies, regardless of obesity. Endothelin-2 (ET-2) is a recently identified protein that is secreted by ovarian granulosa cells and plays a critical role in ovulation and corpus luteum formation.The mechanisms regulating Edn2 expression in the ovary are not clear and in some cases controversial. Therefore my current research focuses on investigating mechanisms behind abnormal Edn2 expression in HFD exposure. Our central hypothesis is that HFD leads to diminished ovarian estrogen receptor (ER) signaling, with subsequent Edn2 downregulation and impaired ovulation. The knowledge that will be gained from the proposed experiments is critical to understanding the mechanisms behind HFD-induced ovulatory dysfunction. This new knowledge will help me uncover some important clues in previously unexplained ovulatory dysfunction and subfertility and design potential treatment strategies in women in the future.

Dates of funding: 2018-2019
Ovulatory dysfunction is responsible for 25% of cases of subfertility and is frequently present in women with excessive body weight. Specifically, a high-fat intake causes excessive storage of lipid in non-adipose tissue, including the ovary, which can affect its physiological function and result in reproductive dysfunction in women. Recommended daily intake of fat is 20-30% of total calories, but most American women consume a diet containing at least 35%. Therefore, it is important to consider the impact of elevated dietary fat in ovarian dysfunction, especially as diets promoting high fat intake are becoming very popular, some resulting in a significant weight loss. There is theoretically a considerable population of women impacted by HFD-induced reproductive dysfunction of which the burden and mechanistic causes of action are undetermined. One potential reason why HFD causes an abnormal ovulatory function includes changes in genes critical to normal ovarian function. Endothelin-2 (Edn2), which is crucial in ovulation, was the most significantly altered gene upon exposure to HFD in my previous studies, regardless of obesity. Endothelin-2 (ET-2) is a recently identified protein that is secreted by ovarian granulosa cells and plays a critical role in ovulation and corpus luteum formation.The mechanisms regulating Edn2 expression in the ovary are not clear and in some cases controversial. Therefore my current research focuses on investigating mechanisms behind abnormal Edn2 expression in HFD exposure. Our central hypothesis is that HFD leads to diminished ovarian estrogen receptor (ER) signaling, with subsequent Edn2 downregulation and impaired ovulation. The knowledge that will be gained from the proposed experiments is critical to understanding the mechanisms behind HFD-induced ovulatory dysfunction. This new knowledge will help me uncover some important clues in previously unexplained ovulatory dysfunction and subfertility and design potential treatment strategies in women in the future.

Dates of funding: 2018-2019
Ovulatory dysfunction is responsible for 25% of cases of subfertility and is frequently present in women with excessive body weight. Specifically, a high-fat intake causes excessive storage of lipid in non-adipose tissue, including the ovary, which can affect its physiological function and result in reproductive dysfunction in women. Recommended daily intake of fat is 20-30% of total calories, but most American women consume a diet containing at least 35%. Therefore, it is important to consider the impact of elevated dietary fat in ovarian dysfunction, especially as diets promoting high fat intake are becoming very popular, some resulting in a significant weight loss. There is theoretically a considerable population of women impacted by HFD-induced reproductive dysfunction of which the burden and mechanistic causes of action are undetermined. One potential reason why HFD causes an abnormal ovulatory function includes changes in genes critical to normal ovarian function. Endothelin-2 (Edn2), which is crucial in ovulation, was the most significantly altered gene upon exposure to HFD in my previous studies, regardless of obesity. Endothelin-2 (ET-2) is a recently identified protein that is secreted by ovarian granulosa cells and plays a critical role in ovulation and corpus luteum formation.The mechanisms regulating Edn2 expression in the ovary are not clear and in some cases controversial. Therefore my current research focuses on investigating mechanisms behind abnormal Edn2 expression in HFD exposure. Our central hypothesis is that HFD leads to diminished ovarian estrogen receptor (ER) signaling, with subsequent Edn2 downregulation and impaired ovulation. The knowledge that will be gained from the proposed experiments is critical to understanding the mechanisms behind HFD-induced ovulatory dysfunction. This new knowledge will help me uncover some important clues in previously unexplained ovulatory dysfunction and subfertility and design potential treatment strategies in women in the future.