BACKGROUND: Polycystic ovary syndrome (PCOS) is associated with low-grade inflammation, adipocyte hypertrophy, hyperglycemia, increased serum testosterone levels, and reduced lipolysis. This study aimed to investigate the role of interleukin-6 (IL-6) and IL-11 in the pathophysiology of adipocyte hypertrophy in a rat model of PCOS.

MATERIAL AND METHODS: The rat model of PCOS was developed using a subcutaneous injection of dehydroepiandrosterone (DHEA). Histology of the rat ovaries was used to confirm the development of PCOS. Serum levels of testosterone and glucose were measured. Immunohistochemistry, immunofluorescence, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot were performed to measure IL-6 and IL-11 in the rat model of PCOS. Cell proliferation was measured using the cell counting kit-8 (CCK-8) assay.

RESULTS: Serum levels of testosterone and glucose and the expression of IL-6 and IL-11 were significantly increased in the rat model of PCOS via the activation of AKT/STAT3 signaling. Following IL-6 and IL-11 stimulation of mesenchymal adipocytes isolated from adipose tissue, IL-6 and IL-11 induced cell proliferation through the STAT3/AKT signaling pathway.

CONCLUSIONS: In a rat model of PCOS, increased expression of IL-6 and IL-11 was associated with the AKT/STAT3 pathway. Increased levels of IL-6 and IL-11 stimulated adipocytes from adipose tissue of the rat model, which promoted cell proliferation by activating AKT/STAT3 signaling.

Keywords: Adipose Tissue, Interleukin-11, Interleukin-6, Adipocytes, Blood Glucose, Insulin, Insulin Resistance