Medical Discount Blog

THURSDAY, Jan. 31 (HealthDay News) — Scientists think they have discovered a mechanism that prompts early menopause and might account for some infertility problems in women.

PTEN — a gene that's known for suppressing tumor growth — apparently besides keeps immature eggs in the ovary from ripening too quickly. When researchers deleted the PTEN gene in mice, the rodents ran out of their entire supply of eggs while they were still in the mouse equivalent of early adulthood. If ultimately applicable in humans, the revelation could lead to more completely infertility treatments.

"This finding is believed to own broad physiological, clinical and practical significance," said senior study originator Kui Liu, an collaborator professor of medical biochemistry and biophysics at Umea University, in Sweden. The report is published in the Feb. 1 issue of Science.

A woman's ovaries are made up of follicles, each of which contains an oocyte (the germ cell which will eventually give rise to an egg).

Over time, the majority of follicles remain dormant, acting as holding pens for immature oocytes. Some of these dormant follicles, however, slowly move over to the growing active follicle loch, where they are make use of for immediate release and, perhaps, fertilization. Menopause occurs when there are no greater amount of follicles and, therefore, no more oocytes left.

The length of a woman's reproductive lifetime is determined by the size of her follicle pool and the rate at which this pool is depleted.

Until now, scientists have not completely understood what mechanisms are involved in this process.

For this studious mood, Liu and colleagues deleted the PTEN gene in mice and found that these mice produced, at the principally, one normal-sized litter after which they could no longer give birth. They were still in early adulthood (12 to 13 weeks of age) when they experienced this premature ovarian failure.

The similar genetic variation may be responsible for premature ovarian failure in women’s health, the authors stated. And manipulating the PTEN gene could clinch faith for the future.