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• W3081467660 endingPage "118310" @default.
• W3081467660 startingPage "118310" @default.
• W3081467660 abstract "Polycystic ovary syndrome (PCOS) is an endocrinopathy, and it accounts for 75% of non-ovulatory infertile in women of childbearing age. It is clear that obesity, insulin resistance, dyslipidaemia coexist in PCOS. Apelin, as an endogenous ligand of the previously orphan receptor, is an adipokine that secreted by adipose tissue. Apelin and apelin receptors are expressed in many tissues and organ to regulate their physiological functions. Studies have shown that Apelin/apelin-receptor also expressed in ovary such as follicles, granulosa cells. Furthermore, Apelin/apelin-receptor play roles in vascular establishment and hormone metabolism in ovary. These indicate that the Apelin/apelin-receptor play an important role in the development of follicle. Apelin/apelin-receptor are increased in ovary of PCOS, which are associated with abnormal ovarian hormones and function. These are important causes of menstrual cycle disorders and anovulation. Moreover, apelin now appears clearly as a new player in energy metabolism. Apelin can regulate glucose and lipid metabolism but also modulate insulin secretion. And plasma apelin concentrations are elevated in obesity and type 2 diabetes patients. Interestedly, obesity and type 2 diabetes are also companied with polycystic ovary syndrome patients. We speculate apelin/apelin-receptor may play a vital role in pathogenesis of polycystic ovary syndrome, but the underlying mechanisms remain under exploration. Here, we review apelin/apelin-receptor, as a new therapeutic target, have effects on ovarian function and energy metabolism in polycystic ovary syndrome." @default.
• W3081467660 created "2020-09-01" @default.
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• W3081467660 date "2020-11-01" @default.
• W3081467660 modified "2023-10-12" @default.
• W3081467660 title "Apelin/Apelin receptor: A new therapeutic target in Polycystic Ovary Syndrome" @default.
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• W3081467660 doi "https://doi.org/10.1016/j.lfs.2020.118310" @default.
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