ArticleiScience2026
Multi-omics profiling reveals molecular features of visceral adiposity in autonomous cortisol secretion.
Article in iScience, 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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18 authors.
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Abstract
Autonomous cortisol secretion (ACS) from adrenal adenomas increases cardiometabolic risk. Visceral adiposity is a hallmark of ACS. We characterized ACS-associated visceral adiposity using multi-omics profiling of periadrenal adipose tissue and plasma. ACS exhibited higher visceral-to-subcutaneous fat ratio (VSR), adipocyte hypertrophy, and inflammation-related pathway enrichment than non-functioning adrenal tumors. RNA-seq deconvolution and immunohistochemistry indicated increased macrophage infiltration. Plasma steroid metabolomics identified 11-deoxycorticosterone (11-DOC), a mineralocorticoid metabolite, as positively associated with VSR in premenopausal ACS women independent of cortisol. The 11-DOC-associated gene module correlated with inflammation-related pathways, notably macrophage activation. Lipidomics identified ceramides as ACS discriminators, with Cer(d18:1/16:0) most strongly associated with inflammation- and lipid metabolism-related pathways. Mendelian randomization showed genetically predicted plasma Cer(d18:1/16:0) was positively associated with trunk fat mass. These findings identify circulating 11-DOC and adipose ceramide accumulation as molecular features associated with adipose inflammation and visceral adiposity in ACS, providing hypothesis-generating insights that require functional validation.
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