Adipose Tissue Dysfunction in Polycystic Ovary Syndrome
Authors' conclusion
AT dysfunction, more than AT distribution and excess adiposity, contributes to the metabolic and inflammation abnormalities of PCOS. Nonetheless, many studies provided contradictory, unclear, or limited data, highlighting the urgent need for additional research in this important field.
Study context
- Population
- Studies of adipose tissue (AT) dysfunction in polycystic ovary syndrome (PCOS), prioritising those assessing AT function directly; therapies targeting AT dysfunction
- Outcome
- Mechanisms of AT dysfunction in PCOS
Pooled result
As reported in the abstract
- Mechanisms identified: dysregulated storage capacity, hypoxia and hyperplasia; impaired adipogenesis; impaired insulin signaling and glucose transport; dysregulated lipolysis and NEFA kinetics; adipokine and cytokine dysregulation and subacute inflammation; epigenetic dysregulation; mitochondrial dysfunction, endoplasmic reticulum and oxidative stress
- Decreased glucose transporter-4 expression and content in adipocytes, with decreased insulin-mediated glucose transport in AT, was a consistent abnormality despite no alterations in insulin binding or IRS/PI3K/Akt signaling
- Adiponectin secretion in response to cytokines/chemokines is affected in PCOS vs controls
- Epigenetic modulation via DNA methylation and microRNA regulation appears important in AT dysfunction in PCOS
Original publication
Adipose Tissue Dysfunction in Polycystic Ovary Syndrome. J Clin Endocrinol Metab. Published 17 June 2023. doi:10.
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