Modulation of GABA by sodium butyrate ameliorates hypothalamic inflammation in experimental model of PCOS

Polycystic ovarian syndrome (PCOS) is a known endocrine disorder that has affected many women of childbearing age, and is accompanied by various neurodegenerative conditions.

Hence, this study investigates the impact of butyrate in reversing hypothalamic-related disorder, possibly through γ aminobutyric acid (GABA) in a rat model of PCOS.

Eight-week-old female Wistar rats were allotted into four groups (n = 5), which include control, butyrate, letrozole, and letrozole + butyrate groups.

PCOS was induced by administering 1 mg/kg of letrozole (oral gavage) for 21 days.

After confirmation of PCOS, 200 mg/kg of butyrate (oral gavage) was administered for 6 weeks.

Rats with PCOS were characterized by elevated levels of plasma insulin and testosterone.

Increases in plasma and hypothalamic triglyceride levels, inflammatory biomarker (SDF-1), apoptotic marker (caspase-6), and decreased plasma GnRH were observed.

Additionally, a decrease in hypothalamic GABA was revealed.

Nevertheless, the administration of butyrate attenuated these alterations.

The present study suggests that butyrate ameliorates hypothalamic inflammation in an experimental model of PCOS, a beneficial effect that is accompanied by enhanced GABA production.