A transcriptional and cellular exploration of obesity and type II diabetes in human adipose tissues.

In 58 people with obesity, single-cell and cellular profiling links T2D status to depot-specific remodeling of omental stromal cells, including lipid-overload inflammation in endothelial cells.

• Why it matters: Obesity is strongly associated with T2D, yet some obese individuals avoid it; the biological basis of this vulnerability is not well defined.
• What they did: The study recruited 58 individuals with obesity with or without T2D and profiled paired omental and subcutaneous adipose using single-cell RNA sequencing (n=10), flow cytometry under basal and stimulated conditions (n=42), and histology (n=17). It also measured chemokines and performed flow cytometry in paired whole blood.
• The result: Omental stromal reprogramming centered on mesothelial and endothelial cells, with mesothelial and IGFBP2+ cells showing a fibrotic, epithelial-mesenchymal transition-like phenotype and omental endothelial cells showing a lipid-overload, inflammatory, antigen presentation profile in T2D. Divergent innate T cell and macrophage phenotypes across depots suggest compensatory networks that may be targeted therapeutically.

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