Publications by authors named "Helen Diane Mason"
Context: Hyperinsulinemia in polycystic ovary syndrome is widely treated with the insulin sensitizer metformin, which, in addition to its systemic effects, directly affects the ovarian insulin-stimulated steroidogenesis pathway.
Objective: Our aim was to investigate the interaction of metformin with the other insulin-stimulated ovarian pathway, namely that leading to glucose uptake.
Design: Human granulosa-luteal cells were cultured with metformin (10(-7) M), insulin (10 ng/ml) or metformin and insulin (met + ins) combined.
Metformin is commonly used to treat women with polycystic ovary syndrome, but its precise mechanism of action is unclear, and it even appears to have direct ovarian effects. At the cellular level, it may act either via an insulin-dependent pathway or an independent pathway by activating AMP-activated protein kinase (AMPK). In the ovary, metformin directly decreased estradiol and progesterone production by human granulosa cells, and inhibition of progesterone production by metformin in rat granulosa cells caused an increase in phosphorylated AMPK (pAMPK).
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- Metformin is a medicine often prescribed for a condition called polycystic ovary syndrome, and it helps with issues related to insulin resistance.
- Scientists found that metformin not only helps with insulin but also slows down the production of certain hormones in the ovaries, specifically estradiol.
- The study showed that metformin lowers the activity of an enzyme needed to make these hormones, and this happens through a specific cell signaling pathway that was affected when they added a special chemical to block it.