THBS1 links fat-cell changes to inflammation in a human tissue atlas
A cellular map of abdominal fat linked THBS1-rich cell populations with fibrosis and inflammation in obesity and diabetes. The single peer-reviewed study examined tissue from 21 Korean participants and followed up with cell, tissue and mouse experiments. Blocking THBS1 reduced these changes in experimental systems. The small human sample and the protein’s production in other tissues complicate its interpretation as a clinical marker.
Science··Midday
A cell map of visceral fat
Gene activity in 86,000 cell nuclei revealed changes in abdominal fat across obesity and diabetes in a single peer-reviewed study. Surgical tissue came from 21 Korean participants: eight people in the lean group, five in the obesity group and eight in the obesity-with-diabetes group. The researchers distinguished eight broad cell types. THBS1, a secreted protein involved in tissue remodeling, marked subsets of fat cells and fat stem cells with prominent inflammatory and fibrosis-related features. Those populations were more common in the metabolically affected groups.[1]
Cell communication promotes fibrotic changes
The team investigated the association using human primary cells, cultured tissue pieces and mouse experiments. Results supported a route through macrophages, immune cells that can alter their surroundings. THBS1 promoted activation of TGFβ, a signaling protein involved in fibrosis, in this cellular interaction. Blocking THBS1 with an antibody or peptide reduced inflammatory and fibrotic features in experimental systems. The atlas also found a shift between macrophage populations: an inflammatory subset increased while another associated with tissue maintenance declined. These functional experiments supplemented the human tissue comparisons rather than establishing treatment benefit in patients.[1]
Blood associations need broader testing
A separate participant group linked plasma and adipocyte THBS1 levels with body mass index and HbA1c, a measure related to longer-term blood glucose. Circulating THBS1 also comes from other tissues, making a blood measurement difficult to attribute specifically to fat. The small atlas cohort could not support reliable comparisons by sex, and its Korean-only composition limits generalization. Tissue processing groups also overlapped with metabolic categories, leaving potential technical effects. Diagnostic performance and clinical benefit from targeting THBS1 were not established.[1]
