# PPARγ Mediates Transdifferentiation of CX3CR1+-Derived Cells into Adipocytes

## TL;DR

This study shows that CX3CR1-derived cells can turn into fat cells, with PPARγ playing a key role in this process.

## Contribution

The study reveals that PPARγ mediates the transdifferentiation of CX3CR1-derived cells into adipocytes.

## Key findings

- CX3CR1-derived cells can transdifferentiate into adipocytes.
- Cold exposure promotes this transdifferentiation, while a high-fat diet inhibits it.
- PPARγ is identified as a key regulator of this process.

## Abstract

Transdifferentiation of one cell type into another occurs under normal physiological conditions. Adipose tissue is an important metabolic and endocrine organ involved in the onset and progression of various diseases. Previous studies have shown that fibroblasts can transdifferentiate into adipocytes. Here, we demonstrate that CX3CR1-derived cells can also transdifferentiate into adipocytes. Additionally, RFP+ SVF cells and mature adipocytes were identified in different adipose tissues of Cx3cr1cre: Rosa26Td mice. Cold exposure enhances the adipogenic transdifferentiation of RFP+ cells, whereas a high-fat diet (HFD) inhibits this process. Mechanistically, we found that PPARγ regulates transdifferentiation, suggesting its role in the differentiation of CX3CR1-derived cells into adipocytes, thus offering new insights into the origin of adipocytes in the body.