ArticleAdipocyte2026
Multi-omics integration reveals convergent extracellular matrix remodelling and lipid metabolic reprogramming as central axes of adipocyte differentiation from mouse embryonic stem cells.
Article in Adipocyte, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Adipogenesis from mouse embryonic stem cells (mESCs) offers a tractable model for dissecting early adipocyte commitment, yet the mechanisms coordinating this transition across multiple biological layers remain incompletely understood. Here we present the first simultaneous five-layer multi-omics characterization of mESC-derived adipocyte differentiation, integrating transcriptomics, proteomics, secretomics, lipidomics, and metabolomics from matched adipogenic (Pos) and non-differentiating (Neg) cell populations at day 30. Applying Multi-Omics Factor Analysis (MOFA+), we identified a dominant shared latent axis that perfectly segregated Pos from Neg cells across all five views. Layer-specific functional enrichment converged on two principal biological axes: ECM remodeling - encompassing collagens, laminins, thrombospondins, and lysyl oxidases - and lipid metabolic reprogramming, with phospholipid and glycerolipid metabolic processes dominating the lipidomics/metabolomics layer. Ensemble Machine Learning Feature Ranking (EMFR) identified a secreted factor (Scpep1; importance score 0.90) as the top-ranked discriminatory feature. Network analysis revealed indirect ECM-lipid connectivity mediated by four bridging nodes (Plod1, Thbs2, Plg, Pmp22) through a hub subnetwork of phospholipid-metabolizing enzymes. Targeted qPCR validation of six candidate regulators (Itga5, Igfbp6, Pik3cg, Lpl, Acer3, Sirt1) confirmed RNA-seq concordance. These findings establish convergent ECM remodeling and lipid metabolic reprogramming as central axes of adipocyte identity acquisition from mESCs.
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