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Role of Liver Fatty Acid-Binding Protein (LFABP) in Adipose Tissue Metabolism

GSE277001 Mus musculus (mouse) RNA-seq (gene expression) 30 samples Submitted 2025/06/18 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 30 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
30 samples
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Novel Hyperplastic Expansion of White Adipose Tissue Underlies the Metabolically Healthy Obese Phenotype of Male LFABP Null MiceCells · 2025
Summary (written by the submitters)
Obesity and adipose tissues quality are important risk factors for the development of type 2 diabetes and metabolic syndrome; this risk is related to intrinsic differences in the behavior of adipocytes in different fat depots. We have shown that the liver fatty acid-binding protein null (LFABP-/-) mouse is a model of the ‘metabolically healthy obese’ (MHO) state.
Read the full summary ↓
Here, we demonstrate that the LFABP-/- mouse is a novel model of hyperplastic subcutaneous adipose tissue (SAT). LFABP-/-mice fed a high-fat diet (HFD) for 12 weeks gained 27% more weight (BW, g: 43.6 LFABP-/- vs 34.4 WT, P<0.001, n=10) and their fat mass was almost double (Fat, g: 15.4 LFABP-/-vs8.3 WT, P<0.001, n=10) that of WT. Intriguingly, despite the substantial increase in mass, inguinal white adipose tissue (iWAT) adipocyte size was >4-fold smaller (46pL LFABP-/-vs222pL WT per cell, P<0.001, n=5) and adipocyte number was 5-fold higher (23.6 LFABP-/-vs4.7 WT x 106, P=0.001, n=5) in the iWAT of LFABP-/-compared to WT mice. Upon obesity development, Lfabp deletion results in transcriptomic differences that include large effects on cholesterol biosynthesis and extracellular matrix (ECM) remodeling, likely leading to tissue growth and a state of ‘adaptive fibrosis’ and ‘homeostatic adipogenesis’ for safe excess energy storage. Since LFABP is not expressed in adipose tissues, these results suggest that its ablation promotes interorgan signaling that may limit hypertrophy and drive hyperplasia in expansion of potentially metabolically beneficial SAT, contributing to the MHO phenotype of the LFABP-/-mouse.
Published in
Novel Hyperplastic Expansion of White Adipose Tissue Underlies the Metabolically Healthy Obese Phenotype of Male LFABP Null Mice
Diolintzi A, Zhou Y, Fomina A et al. · Cells 2025 · PMID 40497936 · doi:10.3390/cells14110760
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE277001_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1160201 and SRA study SRP532282. Searching any of these in the dataset finder brings you back here.

Samples in this study

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