# Regulation of adipose lineage plasticity in obesity

> **NIH NIH R03** · UNIVERSITY OF ILLINOIS AT CHICAGO · 2021 · $119,925

## Abstract

Title: “Regulation of adipose lineage plasticity in obesity”
Project Summary/Abstract
A potential therapeutic target to curb the global obesity and diabetes epidemic is thermogenic beige fat within
white adipose tissue. Unlike white adipocyte which stores fat, beige adipocyte absorbs sugar and fat from the
blood and then burns it. Recent studies indicate that beige adipocytes are present in adult human, and their
activities are correlated with a metabolically healthy phenotype. Due to its promise to reduce adiposity and
improve insulin sensitivity, various molecular cues to induce beige adipocyte lineage have been extensively
investigated. However, most of these studies focus on young and healthy adult. Relatively little work has been
done investigating the white and beige adipocyte plasticity and their regulation in obese and old subjects, who
constitutes a large percentage of the obesity-diabetes epidemic. Our long-term goal is to understand adipose
lineage development and their plasticity in health and disease. During the K01 award period, we identified a
perivascular smooth muscle actin (Sma) positive adipocyte progenitor cells (APCs) that is capable of generating
both white and beige adipocytes. Mechanistically, we identified a platelet-derived growth factor receptor α
(Pdgfrα) as a novel regulator of white and beige adipocyte switch, the deletion of which leads to beige lineage
maintenance in high fat diet induced obesity. We observed that mutant mice with the perdurance of beige
adipocytes were resistant to weight gain, improved glucose metabolism, and had better overall energy
expenditure. We hypothesize that this would be a novel approach to utilize white-to-beige fat switch as a therapy
for diet-induced and age-associated obesity. We will test the hypothesis that modulating APC Pdgfrα activity will
alter adipose lineage plasticity in obesity with the following 2 aims: 1: Determine the APC-intrinsic role of Pdgfrα
in diet-induced obesity; and 2: Determine the mechanisms by which Pdgfrα controls beiging potential in obese
and old mice. In this proposal, we plan to leverage our innovative experimental models to understand how Pdgfrα
controls the fate of white and beige APCs, and how this increased beige life span regulates adiposity and
metabolism in obese and old animals. It is hoped that the results of this proposal will shed light on novel molecular
targets and cellular processes that can be therapeutically exploited to improve energy expenditure for the
prevention and treatment of obesity and its associated metabolic disorders, including diabetes. This R03
application's proposed aims are based on strong preliminary data generated from the ongoing K01, will allow
developing the rationale and provide additional preliminary data for an R01 application in this area.

## Key facts

- **NIH application ID:** 10110174
- **Project number:** 1R03DK127149-01
- **Recipient organization:** UNIVERSITY OF ILLINOIS AT CHICAGO
- **Principal Investigator:** Yuwei Jiang
- **Activity code:** R03 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $119,925
- **Award type:** 1
- **Project period:** 2021-02-15 → 2022-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10110174

## Citation

> US National Institutes of Health, RePORTER application 10110174, Regulation of adipose lineage plasticity in obesity (1R03DK127149-01). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10110174. Licensed CC0.

---

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