Brown adipose tissue activation with ginsenoside compound K ameliorates polycystic ovary syndrome

• DOI: 10.1111/bph.15909
• Publication Date: 2022-06-25T16:39:32Z
• Authors: Rongcai Ye; Chunlong Yan; Huiqiao Zhou; Chuanhai Zhang; Yuanyuan Huang; Meng Dong; Hanlin Zhang; Jun Lin; Xiaoxiao Jiang; Shouli Yuan; Li Chen; Rui Jiang; Ziyu Cheng; Kexin Zheng; Anni Yu; Qiaoli Zhang; Lin‐hu Quan; Wanzhu Jin
• Keywords: 0303 health sciences; Ginsenosides; Dehydroepiandrosterone; Rats; 3. Good health; Disease Models, Animal; Mice; 03 medical and health sciences; Adipose Tissue, Brown; Animals; Humans; Female; Polycystic Ovary Syndrome

Background and PurposePolycystic ovary syndrome (PCOS) is a common metabolic and endocrine disease affecting women of reproductive age. Due to its complex aetiology, there is no currently effective cure for PCOS. Brown adipose tissue (BAT) activity is significantly decreased in PCOS patients, and BAT activation has beneficial effects in animal models of PCOS. Here, we investigated the effect of ginsenoside compound K (CK) in an animal model of PCOS and its mechanism of BAT activation.Experimental ApproachPrimary brown adipocytes, 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 effect of CK on overall energy metabolism. Oestrous cycle, serum sex hormone, ovarian steroidogenic enzyme gene expression and ovarian morphology were also evaluated following CK treatment.Key ResultsOur 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, oestrous 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 up‐regulated 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 ImplicationsIn 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.