# Physiological and functional effects of beta-cell-specific inactivation of the PGE2 receptor EP3

> **NIH NIH F31** · VANDERBILT UNIVERSITY · 2021 · $11,452

## Abstract

Project summary/Abstract
Type 2 diabetes is a major health concern in the United States. It occurs when individuals fail to compensate
for an increased demand for insulin from the pancreatic β cells. The prostaglandin E receptor EP3 (encoded by
Ptger3), which responds to prostaglandin E2 (PGE2), has been shown to inhibit insulin secretion. EP3 is
upregulated in diabetic individuals and with age. Data from our lab has demonstrated that ex vivo
pharmacological inhibition of EP3 increases β cell mass and survival. The role of EP3 specifically in the β cell
has not been examined. I propose using a β-cell-specific EP3 KO mouse model to determine the effect of EP3
inactivation in the context of high fat diet. In addition, FoxM1 is a transcription factor necessary for β cell
proliferation. FoxM1 levels decrease with age while EP3 levels increase. In this proposal, I outline experiments
to elucidate what role, if any, FoxM1 has in regulating Ptger3 expression.

## Key facts

- **NIH application ID:** 10248348
- **Project number:** 5F31DK127613-02
- **Recipient organization:** VANDERBILT UNIVERSITY
- **Principal Investigator:** Ashley A Christensen
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $11,452
- **Award type:** 5
- **Project period:** 2020-09-01 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10248348

## Citation

> US National Institutes of Health, RePORTER application 10248348, Physiological and functional effects of beta-cell-specific inactivation of the PGE2 receptor EP3 (5F31DK127613-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10248348. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*