Alleviation of adipose-hepatic glycolipid dysregulation by acetate in experimental PCOS model is associated with NF-κB/NLRP3 repressionKehinde S Olaniyi, Stephanie E. Areloegbe
- Physiology (medical)
- General Medicine
This study hypothesized that acetate breaks the vicious cycle driving adipose-hepatic metabolic dysregulation in a rat model of PCOS, possibly by suppression of NF-κB/NLRP3 inflammasome. Female Wistar rats (eight-week-old) were randomly allocated into 4 groups of n=six/group, which received vehicle, sodium acetate (200 mg), letrozole (1 mg/kg) and letrozole plus sodium acetate respectively. The animals were treated by oral gavage, once daily for a period of 21 days. The PCOS animals were insulin resistant, hyperandrogenic and hypoestrogenic with decreased sex hormone binding globulin. In addition, the hepatic tissue had increased lipid profile and decreased glycogen synthesis, while the adipose tissue showed decreased lipid profile with elevated glycogen synthesis. Besides, the results also showed increased malondialdehyde, γ-glutamyl transferase, lactate dehydrogenase, inflammatory mediators with corresponding decrease in antioxidant defense in the hepatic and adipose tissues. Immunohistochemical evaluation also demonstrated severe expression with BAX/NLRP3 antibodies. Nonetheless, concomitant acetate supplementation attenuated these derangements. The present data collectively suggest that acetate ameliorates adipose-hepatic glycolipid dysregulation in experimental PCOS model by attenuating androgen excess and NF-κB/NLRP3 immunoreactivity.