Advances in Adipose-Tissue Immunity and Metabolism in Polycystic Ovary Syndrome

doi:10.12280/gjfckx.20250868

Abstract

Abstract:

Polycystic ovary syndrome (PCOS) is a prevalent endocrinopathy among reproductive-age women. Adipose-tissue dysfunction constitutes the pivotal axis linking reproductive-endocrine derangements to metabolic dysregulation; the resulting chronic low-grade inflammation and insulin resistance perpetuate a vicious cycle with hyperandrogenism. The adipose-tissue immune microenvironment in PCOS is markedly perturbed: an imbalance in M1/M2 macrophage polarization leads to extensive infiltration of pro-inflammatory M1 macrophages, and the newly identified inflammatory and metabolically activated macrophage (iMAM) subset may act as a key disease-progression driver. Metabolic disequilibrium traps adipose tissue in a loop of lipotoxicity and oxidative stress, while adipokine secretion is dysregulated, manifesting as aggravated leptin resistance and decreased adiponectin levels. These pathological changes seriously impair ovarian steroidogenesis, ovulation function, and endometrial receptivity, thereby compromising fertility. Among emerging therapeutic strategies, glucagon-like peptide-1 receptor agonists promote adipose-tissue browning and reestablish immune homeostasis, and exosomes derived from adipose mesenchymal stem cells deliver specific microRNAs for precise modulation, providing a theoretical basis for individualized interventions targeting the adipose-tissue microenvironment.

Key words: Polycystic ovary syndrome, Adipose tissue, Adipokines, Macrophages, Lipid metabolism disorders

Xiemuxinuer • Simayi, HUANG Ya-nan, ZHANG Man-li, HAN Rui. Advances in Adipose-Tissue Immunity and Metabolism in Polycystic Ovary Syndrome[J]. Journal of International Obstetrics and Gynecology, 2026, 53(1): 78-84.

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