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Monday, 3 October 2016

Women's Breasts 'eat' themselves after they finish breastfeeding – Discovery

Scientists have identified the molecular switch that causes women's breasts to stop producing milk when they stop breastfeeding.  Once lactation is complete, cells in the breasts devour dead cells that are left over from the breastfeeding process. 


Scientists had previously been baffled about how breasts could rapidly transform from milk-making machines back to their natural state in a matter of days.

It is hoped that the new research could provide vital insights into the development of breast cancer. 
'Women's breasts comprise a network of ducts, covered by a layer of fatty tissue,' explains New Scientist.

'During pregnancy, hormonal signals cause epithelial cells lining the ducts to proliferate and form ball-like structures called alveoli, which is where milk is made when the baby is born. 

'However, once women stop breastfeeding, these structures self-destruct – a process that involves massive cellular suicide, and the removal of the debris'. 

While the body is known to remove dead cells through a process called phagocytosis, the scale of such a process would usually cause significant swelling and pain.

This doesn't appear to happen when a woman finishes breastfeeding, and scientists were not sure why until now. 

Epithelial cells - those which line the the ducts in the breasts - effectively 'eat' the dead cells that are left over after breastfeeding.

Researchers set out to investigate whether a protein called Rac1, which is known to be a vital element of milk production, is responsible for the post-breastfeeding transformation.

A study by researchers at Sheffield University deleted the Rac1 gene from female mice and found that their first litter survived, but were undersized.

It was suggested that this could be a result of lower fat and protein levels in the milk.

However, subsequent litters of the mice did not survive.

Without Rac1, the rodents' breasts were flooded with milk and dead cells, causing continuous swelling, which is thought to have inhibited the mice's ability to regenerate cell tissue and produce milk in later pregnancies.

The study shows for the first time that Rac1 is essential for clearing out dead cells and milk when lactation is over.  

'Given this new role for Rac1 in the removal of excess or dead cells, thereby suppressing inflammation the current study also identifies a potential role for Rac1 in breast cancer that is yet to be explored,' Matthew Naylor, a cancer specialist at the University of Sydney in Australia told New Scientist.

The study was published in the journal Developmental Cell.  




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