Traditional Chinese Medicine formula FTZ protects against polycystic ovary syndrome through modulating adiponectin-mediated fat-ovary crosstalk in mice.

ETHNOPHARMACOLOGICAL RELEVANCE: FuFang ZhenZhu TiaoZhi (FTZ) is a hospitalized traditional Chinese medicine herbal formula with documented metabolic benefits. Polycystic ovary syndrome (PCOS) characterized by ovarian dysfunction and insulin resistance represents one of the most common endocrine disorders in close association with metabolic dysfunction in premenopausal women. AIM OF THE STUDY: The present study aimed to investigate the preventive effect of FTZ on letrozole-induced experimental PCOS and its associated insulin resistance in mice. MATERIALS AND METHODS: Prepubertal female mice in the experimental groups (letrozole and FTZ) received continuous infusion of letrozole (50 µg/day) for 35 days. FTZ was administrated to mice by oral gavage daily at dosage of 2.892 g/kg body weight for 5 weeks. All groups of mice were fed a high-fat diet (HFD). Ovary and adipose tissue were collected from all mice after 5 weeks and adiponectin, testosterone, estradiol, and luteinizing hormone level determined. RESULTS: Letrozole-induced morphological changes in the ovary, including a decreased number of corpora lutea and antral follicles, and increased cystic follicles, were significantly attenuated in FTZ-treated mice. Additionally, FTZ treatment notably reversed PCOS-related disruption of estrous status. PCOS-related insulin resistance was markedly alleviated. Mechanistically, FTZ treatment notably enhanced circulating level and transcriptional abundance of adiponectin in adipose tissue, thereby orchestrating fat-ovary crosstalk. CONCLUSIONS: Our data collectively demonstrate that FTZ exerted preventive benefits in an experimental model of PCOS, at least partially by potentiating the production of adiponectin from adipose tissues. This suggests that FTZ is a promising treatment for PCOS.

Liver-adipose tissue crosstalk: A key player in the pathogenesis of glucolipid metabolic disease.

Glucolipid metabolic disease (GLMD), a complex of interrelated disorders in glucose and lipid metabolism, has become one of the leading chronic diseases causing public and clinical problem worldwide. As the metabolism of lipid and glucose is a highly coordinated process under both physiological and diseased conditions, the impairment in the signals corresponding to the metabolism of either lipid or glucose represents the common mechanism underlying the pathogenesis of GLMD. The liver and adipose tissue are the major metabolic organs responsible for energy utilization and storage, respectively. This review article aims to summarize the current advances in the investigation of the functional roles and the underling mechanisms of the interplay between the liver and adipose tissue in the modulation of GLMD development. Fibroblast growth factor 21 (FGF21) and adiponectin represent the two major hormones secreted from the liver and adipose tissues, respectively. FGF21 exerts pleiotropic effects on regulating glucose and lipid homeostasis majorly through inducing the expression and secretion of adiponectin. Therefore, FGF21-adiponectin axis functions as the key mediator for the crosstalk between the liver and adipose tissue to exert the beneficial effects on the maintenance of the homeostasis of energy consumption. The liver- and adipose tissue-derived factors with pleiotropic effects on regulating of lipid and glucose metabolism function as the key mediator for the crosstalk between these two highly active metabolic organs, thereby coordinating the initiation and development of GLMD.