Brown adipose tissue activation by ginsenoside compound K treatment ameliorates polycystic ovary syndrome. - GreenMedInfo Summary

BACKGROUND AND PURPOSE: Polycystic ovary syndrome (PCOS) is a common metabolic and endocrine disease affecting women of reproductive age. Due to its complex etiology, there is no effective cure for PCOS currently. Brown adipose tissue (BAT) activity is significantly decreased in PCOS patients and BAT activation has beneficial effects on PCOS animal models. Here, we investigated the therapeutic effect of ginsenoside compound K (CK) on an animal model of PCOS and its mechanism of BAT activation EXPERIMENTAL APPROACH: Primary brown adipocyte, Db/Db mice and dehydroepiandrosterone (DHEA)-induced PCOS rats were used. The core body temperature, oxygen consumption, energy metabolism related gene and protein expression were assessed to identify the function of CK on energy metabolism. Estrous cycle, serum sex hormone, ovarian steroidogenic enzyme gene expression and ovarian morphology were evaluated following CK treatment.

KEY RESULTS: Our results indicated that CK treatment could significantly protect against body weight gain in Db/Db mice via BAT activation. Furthermore, we found that CK treatment could normalize hyperandrogenism, estrous cyclicity, normalize steroidogenic enzyme expression and decrease the number of cystic follicles in PCOS rats. Interestingly, as a potential endocrine intermediate, C-X-C motif chemokine ligand-14 protein (CXCL14) was significantly upregulated following CK administration. In addition, exogenous CXC14 supplementation was found to reverse DHEA-induced PCOS in a phenotypically similar manner to CK treatment.

CONCLUSION AND IMPLICATIONS: In summary, CK treatment significantly activates BAT, increases CXCL14 expression and ameliorates PCOS. These findings suggest that CK might be a potential drug candidate for PCOS treatment.