The research findings – using female mice – have been made by PhD student Cadence Minge in the University of Adelaide’s Research Centre for Reproductive Health. Her research has also discovered a way to completely reverse the effects of obesity on mouse eggs, enabling afflicted eggs to develop into healthy embryos. "Consuming a diet high in fat causes damage to eggs stored in female ovaries. As a result, when fertilised, these eggs are not able to undergo normal, healthy development into embryos," Minge says.
Minge has discovered that a protein in the cells surrounding, supporting and nourishing the egg – called Peroxisome Proliferator-Activated Receptor gamma (PPARγ) – is the main reason behind diet-induced infertility. "The behaviour of this protein helps to determine the way in which the ovaries sense and respond to fats," Ms Minge says. "Being able to control this protein will be very important in the quest to reverse infertility caused by poor diets."
Minge's research has found that when the protein is selectively targeted with the anti-diabetes drug rosiglitazone the adverse effects of obesity on egg quality are completely reversed. "The drug enables us to switch on the protein, thereby changing the way in which the ovaries sense and respond to fats. Embryo development rates are restored, and the cellular differentiation of the early embryo is improved," Minge says.
However, Minge warns that rosiglitazone should not be seen as a "quick fix" for infertile women. "The rosiglitazone findings are of great significance for scientists researching egg maturation within the ovary. But at this stage, the research findings have only been made in mice. Also, the drug itself can have possible harmful side-effects, and more research is needed to find other, safer ways of activating the protein," she says.
MEDICA.de; Source: University of Adelaide