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Altered circadian clock as a novel therapeutic target for constant darkness-induced insulin resistance and hyperandrogenism of polycystic ovary syndrome
Changing the body’s internal clock to treat insulin resistance and high male hormone levels caused by constant darkness in polycystic ovary syndrome
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Abstract
Arrhythmic expressions of circadian clock genes due to constant darkness induced metabolic and reproductive hallmarks of polycystic ovary syndrome (PCOS) in rats.
- Constant darkness exposure for 8 weeks altered circadian clock gene expressions in rats.
- Decreased BMAL1 levels led to insulin resistance through glucose transporter 4 (GLUT4) modulation.
- Reduced levels of PER1 and PER2 contributed to androgen excess via insulin-like growth factor-binding protein 4 (IGFBP4) and sex hormone binding globulin (SHBG) in the liver.
- Hyperinsulinemia and hyperandrogenism created a feedback loop that promoted abnormal circadian gene expression and apoptosis of ovarian granulosa cells.
- Altered circadian clock gene expressions in darkness-treated rats were similar to those observed in PCOS patients.
- Melatonin treatment improved hyperinsulinemia and hyperandrogenism in darkness-treated rats by influencing BMAL1, PER1, and PER2.
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