Acetate: A therapeutic candidate against renal disorder in a rat model of polycystic ovarian syndrome

Various endocrinometabolic diseases, inclusively polycystic ovarian syndrome (PCOS) has been linked with increased risk of renal dysfunction with attendant cardiovascular disease (CVD) in women of reproductive age. Short chain fatty acids (SCFAs) especially acetate have been suggested as an immunometabolic modulator. However, the impact of SCFAs, particularly acetate on renal disorder in PCOS individuals is unknown. The present study therefore hypothesized that acetate would circumvent renal dysfunction in a rat model of PCOS, probably by suppressing NF-kappa B-dependent mechanism. Eight-week-old female Wistar rats were randomly distributed into four groups (n = 6), which received vehicle, sodium acetate (200 mg/kg), letrozole (1 mg/kg) and letrozole plus sodium acetate, respectively. The administrations were done by oral gavage once daily for a duration of 21 days. Animals with PCOS showed insulin resistance, lipid dysmetabolism, hyperandrogenism, hyperleptinemia and hypoadiponectinemia. Besides, the result also revealed increased renal malondialdehyde, lactate production, inflammatory mediators (NF-kappa B and TNF-alpha), urea and creatinine concentration. Immuno-histochemical evaluation of renal tissue also demonstrated severe expression of apoptosis and inflammation with BAX/NLRP3 antibodies. However, supplementation with acetate significantly attenuated these anomalies. Collectively, the present results suggest that acetate abolishes renal dysfunction in experimentally induced PCOS animals by attenuating androgen excess, apoptosis, oxidative stress and NF-kappa B/NLRP3 immunoreactivity.

Automated summary

This study investigated the impact of short chain fatty acid acetate on renal disorder in polycystic ovarian syndrome (PCOS). The results showed that supplementation with acetate attenuated renal dysfunction in PCOS rats by reducing androgen excess, apoptosis, oxidative stress, and NF-kappa B/NLRP3 immunoreactivity.