The adiponectin agonist, AdipoRon, inhibits steroidogenesis and cell proliferation in human luteinized granulosa cells

During obesity, excess body weight is not only associated with an increased risk of type 2-diabetes, but also several other pathological processes, such as infertility. Adipose tissue the largest endocrine organ that produces adipokines, including adiponectin. Adiponectin has been reported to control fertility through hypothalamic–pituitary–gonadal axis, and folliculogenesis in ovaries. In this study, we focused on a recent adiponectin-like synthetic agonist called AdipoRon, its action human luteinized granulosa cells. We demonstrated AdipoRon activated adenosine monophosphate-activated protein kinase (AMPK) peroxisome proliferator-activated receptor alpha (PPAR) signalling pathways A 25 ?M stimulation reduced cell proliferation by inducing cycle arrest G1, PTEN p53 pathway activation. addition, perturbed metabolism decreasing mitochondrial activity ATP production. cells, phosphodiesterase activity, leading drop cyclic monophosphate (cAMP) production, aromatase expression oestrogens secretion. conclusion, impacted altering function, via steroid production proliferation. This may have applications for improving ovarian function metabolic disorders or cancers.