Adipose-androgen crosstalk in polycystic ovary syndrome: mechanisms and therapeutic implications.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic models without systematic review methodology or original empirical data.
PubMed 41476920 · doi:10.3389/fendo.2025.1731179
What was done
This review synthesized mechanistic literature examining the bidirectional interactions between adipose tissue dysfunction and hyperandrogenism in polycystic ovary syndrome (PCOS). It evaluated how visceral adiposity, insulin resistance, altered adipokine secretion, and chronic low-grade inflammation interact with ovarian androgen excess, and surveyed current and emerging therapeutic approaches targeting this metabolic-reproductive axis.
What was found
The abstract describes qualitative mechanistic pathways and provides no quantitative data, statistics, or numerical effect sizes. It reports that dysfunctional adipose tissue intensifies insulin resistance, elevates inflammatory markers (such as TNF-α and IL-6), and reduces adiponectin to promote ovarian androgen synthesis. Reciprocally, hyperandrogenism promotes central adiposity, impairs lipogenesis and lipolysis regulation, and alters adipokines (reducing adiponectin and increasing leptin), establishing a self-sustaining cycle of metabolic and reproductive dysfunction.
Why it matters
The paper frames the fat-androgen interaction as a central therapeutic target in PCOS, providing a mechanistic rationale for using metabolic therapies (such as GLP-1 receptor agonists, SGLT-2 inhibitors, and insulin sensitizers) alongside anti-androgens to interrupt disease progression.
Limits
This is a narrative review that reports no primary experimental or clinical trial data. The abstract provides no systematic search methodology, quality appraisal of included studies, or quantitative comparisons of therapeutic efficacy across interventions. Many discussed emerging interventions (such as brown adipose tissue transplantation) remain largely preclinical.