Evidence mapPaperPMID 41260614Full record

ArticleEndocrinology2025

11-Oxygenated Androgens Inhibit Brown Adipose Tissue Differentiation.

Yini Yuan, Jacobie Steenbergen, Afonso de Oliveira Santos Goulart, Alba Sabaté-Pérez, Jenny A Visser

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Article in Endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Yini YuanDepartment of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, 3000 CA, the Netherlands.
Jacobie SteenbergenDepartment of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, 3000 CA, the Netherlands.
Afonso de Oliveira Santos GoulartDepartment of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, 3000 CA, the Netherlands.
Alba Sabaté-PérezDepartment of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, 3000 CA, the Netherlands.ORCID 0000-0001-8257-6406
Jenny A VisserDepartment of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, 3000 CA, the Netherlands.ORCID 0000-0001-7182-3571

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextWomen with polycystic ovary syndrome (PCOS) and PCOS animal models have diminished brown adipose tissue (BAT) activity, potentially contributing to metabolic dysfunction. Besides classical androgens, adrenal 11-oxygenated androgens are elevated in women with PCOS. However, it remains unknown whether these 11-oxygenated androgens affect BAT metabolism.

objectiveTo study the effects of 11-ketotestosterone (KT) and 11-ketodihydrotestosterone (KDHT) on BAT metabolism.

methodsThe female mouse brown adipocyte cell line T37i was treated with increasing concentrations (0.1-10 µM) of testosterone (T), dihydrotestosterone (DHT), KT, or KDHT during or after differentiation. In addition, female mice received a daily injection of vehicle, DHT, KT, or KDHT (100 µg) for 1 day or 1 week. Adipose depots were collected for RNA sequencing (RNAseq) analysis and Gene Set Enrichment Analysis (GSEA).

resultsDuring differentiation, T, KT, DHT, and KDHT treatment of T37i cells dose-dependently reduced lipid droplet accumulation, and downregulated mRNA expression of adipogenic markers by up to 50%, with KDHT having the weakest effect. In mature T37i cells, only the high concentrations of these androgens exhibited inhibitory effects. RNAseq analysis revealed that DHT exposure induced the most differentially regulated genes in BAT, followed by KT and KDHT treatment. GSEA indicated that 1-day treatment with DHT and KT, but not KDHT, resulted in the downregulation of metabolic pathways in BAT.

conclusion11-Oxygenated androgens at high concentrations directly inhibit brown adipocyte differentiation in vitro and KT acutely downregulates BAT metabolic transcriptome in vivo, a result not observed with KDHT. These findings suggest that elevated 11-oxygenated androgens may impair BAT function, contributing to metabolic complications associated with hyperandrogenic conditions, including PCOS.

Indexed as

Adipocytes, BrownAdipose Tissue, BrownAndrogensCell DifferentiationTestosteroneAdipogenesisAnimalsCell LineDihydrotestosteroneFemaleMiceMice, Inbred C57BLPolycystic Ovary Syndrome11-ketotestosteroneAndrogensDihydrotestosteroneTestosterone11-oxygenated androgensBATmetabolismPCOS

Identifiers

PMID41260614
PMCPMC12658366

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.