# Identification and Analysis of Key lncRNAs for Adipose Differentiation

**Authors:** Xiujie Xie, Tianyu Li, Bohang Zhang, Junxiong Liao, Xing Zhang, Jing Gao, Xiaofang Cheng, Tiantian Meng, Yongjie Xu, Pengpeng Zhang, Cencen Li

PMC · DOI: 10.3390/biology15010087 · Biology · 2025-12-31

## TL;DR

This study identifies new long non-coding RNAs that may regulate fat cell differentiation and could help treat obesity by promoting fat browning.

## Contribution

The study identifies novel lncRNAs associated with adipocyte browning and differentiation using transcriptomic data from mouse adipose tissues.

## Key findings

- 794 novel lncRNAs and 1499 differentially expressed genes were identified across white, brown, and beige adipose tissues.
- Two lncRNAs, MSTRG.12661 and MSTRG.17758, are linked to extracellular matrix organization and fatty acid oxidation.
- The identified lncRNAs may serve as new therapeutic targets for obesity treatment through white adipose tissue browning.

## Abstract

Long non-coding RNAs (lncRNAs) are well-recognized regulators of adipocyte differentiation and metabolic processes. However, their specific roles in adipocyte browning remain poorly characterized. To address this knowledge gap, we performed transcriptomic analyses on publicly available RNA-seq datasets of mouse white (WAT), brown (BAT), and beige (BeAT) adipose tissues; these datasets were retrieved from the EMBL-EBI database under the accession number E-MTAB-2624. Through a sophisticated bioinformatics analysis pipeline, we ultimately identified 794 novel lncRNAs and 1499 differentially expressed genes (DEGs), among which 95 were shared across all three adipocyte types. Among these novel lncRNAs, two specific lncRNAs, MSTRG.12661 and MSTRG.17758, were found to be tightly associated with key biological processes, including extracellular matrix organization and fatty acid oxidation; functional prediction further indicates their potential involvement in adipocyte type-specific differentiation. To conclude, our study identified novel lncRNAs potentially involved in regulating adipocyte differentiation, providing new candidate targets for treating obesity by inducing white adipose tissue browning.

Recent studies have demonstrated that the abundance of brown adipose tissue is inversely associated with obesity in humans. Promoting the browning of white adipocytes therefore represents a promising therapeutic strategy for obesity treatment. LncRNAs are known regulators of adipocyte differentiation and metabolic processes. However, their specific roles in adipocyte browning remain poorly characterized. In this study, we performed transcriptomic analyses using publicly available RNA-seq datasets of mouse white, brown and beige adipose tissues from the EMBL-EBI database. Our analytical workflow included raw data quality control, alignment to the reference genome, transcript assembly, coding potential assessment and differential expression analysis. Functional annotation was conducted through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Key lncRNAs were further validated via Reverse Transcription Quantitative PCR (RT-qPCR). We identified 794 novel lncRNAs and 1499 DEGs, among which 95 were common across all three adipocyte types. Two lncRNAs, MSTRG.12661 and MSTRG.17758, were found to be closely related to critical biological processes, including extracellular matrix organization and fatty acid oxidation. Functional prediction suggests their potential involvement in adipocyte type-specific differentiation. In conclusion, our study reveals novel lncRNAs that may regulate adipocyte differentiation, offering new candidate targets for obesity treatment via induction of white adipose tissue browning.

## Linked entities

- **Diseases:** obesity (MONDO:0011122)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Diseases:** obesity (MESH:D009765)
- **Chemicals:** fatty acid (MESH:D005227)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12785126/full.md

## References

38 references — full list in the complete paper: https://tomesphere.com/paper/PMC12785126/full.md

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Source: https://tomesphere.com/paper/PMC12785126