In rats with a laboratory-induced form of PCOS, the level of a specific inflammatory marker called IL-6 in the blood was not higher than in rats without PCOS, when both groups ate the same diet.
Mechanism
Synthesis from 1 study
Even though these rats had PCOS caused by extra testosterone and insulin problems, their bodies didn't start making more of the inflammation signal IL-6. This means the way PCOS was created here doesn't turn on the usual biological switches that make IL-6 rise, unlike in other models or conditions.
Most probable mechanism
Even though the rats were given extra testosterone and became insulin resistant, their bodies didn't produce more of the inflammation signal IL-6 than healthy rats. This suggests that the way PCOS was created in these rats doesn't trigger the usual pathways that make the body release this specific inflammation marker.
Testosterone administration induces ovarian dysfunction and insulin resistance without activating macrophage or adipocyte inflammatory signaling pathways
No increase in RAGE receptor activation or NF-κB pathway stimulation occurs in PCOS-induced rats on a standard diet
IL-6 transcription and secretion from immune and adipose cells remain at baseline levels despite metabolic disruption
Evidence from Studies
Supporting (1)
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