# Role of 17β-hydroxysteroid dehydrogenase in the hypertension of PCOS

> **NIH NIH P20** · UNIVERSITY OF MISSISSIPPI MED CTR · 2020 · $318,010

## Abstract

PROJECT III: ROLE OF 17Β-HYDROXYSTEROID DEHYDROGENASE IN THE HYPERTENSION OF PCOS.
SUMMARY
Polycystic Ovary Syndrome (PCOS) is characterized by increases in plasma androgens and/or hirsutism,
irregular menstrual periods, ovarian cystic morphology and infertility. Although the etiology of PCOS is
unknown, one theory is that PCOS may be developmentally programmed due to exposure to prenatal
androgens. PCOS is one of the most common female endocrine disorders, affecting 5 to 26% of women of
reproductive age depending on ethnicity and lifestyle. Recent attention in women with PCOS in the US has
focused on several metabolic derangements such as obesity, insulin resistance and hypertension. In the US
the prevalence of obesity in PCOS women is up to 80%. Obesity plays a major role in the clinical
manifestations of the syndrome, since weight loss is associated with improved fertility and reductions in
metabolic derangements in PCOS patients. Several lines of evidence indicate that there is a positive
relationship between circulating levels of androgens, obesity, insulin resistance and blood pressure (BP) in
women with PCOS. Whether and how increases in circulating androgens cause obesity, insulin resistance and
hypertension in PCOS women remains poorly understood and is the main focus of this proposal.
 We have established an animal model of PCOS in female rats that mimics many of the metabolic and
cardiovascular abnormalities of women with PCOS. Implantation of dihydrotestosterone (DHT) pellets in
female rats causes an increase in food intake, subcutaneous adipose tissue, insulin resistance, obesity, and
elevated BP, as observed in PCOS women.
 In this proposal we will test the hypothesis that in PCOS, increased plasma androgens via the androgen
receptor cause an increase in food intake leading to obesity that includes an increase in subcutaneous adipose
tissue, and insulin resistance. The combination of increased circulating androgens, obesity and insulin
resistance activate adipose 17β-HSD, resulting in increased adipose androgen synthesis that further increases
circulating androgen levels setting up a vicious cycle. Increased circulating androgens lead to subsequent
activation of the intrarenal renin angiotensin system and elevated blood pressure. This hypothesis will be
tested using an integrative physiological approach using whole animal, cellular, molecular and imaging
methods in the following specific aims: 1) to test the hypothesis that increased circulating androgens via
activation of the androgen receptor promotes obesity with an increase in subcutaneous adipose tissue and
insulin resistance in PCOS; 2) to test the hypothesis that increases in subcutaneous adipose tissue and insulin
resistance lead to activation of 17β-HSD in the subcutaneous adipose tissue, thus further increasing circulating
levels of androgens in PCOS; 3) to test the hypothesis that increased circulating androgens activate the
intrarenal renin-angiotensin system (RAS), shif...

## Key facts

- **NIH application ID:** 9985908
- **Project number:** 5P20GM121334-04
- **Recipient organization:** UNIVERSITY OF MISSISSIPPI MED CTR
- **Principal Investigator:** LICY LORENA YANES CARDOZO
- **Activity code:** P20 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $318,010
- **Award type:** 5
- **Project period:** — → —

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9985908

## Citation

> US National Institutes of Health, RePORTER application 9985908, Role of 17β-hydroxysteroid dehydrogenase in the hypertension of PCOS (5P20GM121334-04). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9985908. Licensed CC0.

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