# The regulation of BRD7 in glucose homeostasis

> **NIH NIH R01** · BOSTON CHILDREN'S HOSPITAL · 2020 · $442,500

## Abstract

PROJECT SUMMARY
Obesity is the major pathology underlying the development of insulin resistance and type 2 diabetes. Despite
extensive research, identifying the molecular link between obesity and type 2 diabetes has been a big
challenge and it still remains elusive. Currently, there is no cure for type 2 diabetes and no therapeutic
treatment methods for obesity. In order to find a therapeutic target, it is important to understand the
pathophysiology of obesity and the molecular mechanism by which insulin resistance develops.
Recently, it has been reported that the expression levels of a protein called bromodomain-containing protein 7
(BRD7) are significantly reduced in the liver of obese mice. Furthermore, it has been shown that restoration of
BRD7 in the liver of obese and diabetic mice reduces blood glucose levels and improves glucose tolerance.
Therefore, it is evident that BRD7 is involved in the regulation of glucose homeostasis. This proposal aims to
investigate a novel molecular mechanism by which BRD7 improves glucose tolerance and insulin sensitivity.
The ultimate goal of this project is to understand whether BRD7 can serve as a novel target to treat type 2
diabetes in obese individuals.
This project addresses several novel mechanistic pathways in insulin signaling. These include understanding
how BRD7 leads to the alteration of insulin receptor signaling in response to insulin, and how hepatic glucose
production and blood glucose levels are regulated by BRD7. In Aim 1, genetically engineered mouse models
will be used to define the role of BRD7 in the insulin signaling pathway. The outcome of these experiments will
reveal a novel mechanism by which insulin receptor signaling is controlled. In Aim 2, several mouse models
and cell lines will be utilized to understand the regulation of glycogen and lipids by BRD7. The results of
experiments under Aim 3 will provide a better understanding of the regulation of BRD7. Successful outcomes
of this proposal will improve scientific knowledge in the field of type 2 diabetes, and also suggest an alternative
way to not only treat type 2 diabetes, but also prevent the development of insulin resistance and glucose
intolerance in obese patients.

## Key facts

- **NIH application ID:** 9979849
- **Project number:** 5R01DK118244-02
- **Recipient organization:** BOSTON CHILDREN'S HOSPITAL
- **Principal Investigator:** Sang Won Park
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $442,500
- **Award type:** 5
- **Project period:** 2019-07-17 → 2024-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9979849

## Citation

> US National Institutes of Health, RePORTER application 9979849, The regulation of BRD7 in glucose homeostasis (5R01DK118244-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9979849. Licensed CC0.

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