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How mammals fuel milk production may have implications for cancer

A new study in the December issue of the journal Cell Metabolism, published by Cell Press, offers insight into the manner in which the mammary glands of mammals meet the incredible metabolic demands of milk production. As the normal pathways of breast development undoubtedly affect breast cancer, the findings may have therapeutic implications, the researchers said.

The researchers found that one of three isoforms of the gene known as Akt is specifically required for lactating mice to synthesize sufficient quantities of milk to support their offspring. While the loss of so-called Akt1 does not lead to structural abnormalities, they found, mothers deficient for the gene exhibit a disruption of the coordinated metabolic changes that normally occur at the onset of lactation.

The developmental program that prepares the mammary gland for lactation is among the most critical and highly conserved in mammals, as provision of nutritional support is essential for the survival of offspring, said Lewis Chodosh, lead author of the study at the University of Pennsylvania School of Medicine. Given its remarkable importance, it has been a relatively understudied field.

Our studies demonstrate that Akt1 is required for orchestrating many of the dramatic developmental changes in metabolism that occur in the mammary gland at the transition from pregnancy to lactation.

Although breast cells do not proliferate during lactation after the initial 24 hours, the metabolic demands and synthetic capacity of the lactating mammary gland exceed that of any other tissue, the researchers explained.

The breast is one of the few scenarios in which metabolism isnt tied to the proliferation or growth of cells, Chodosh said. The breast is an unusual organ thats essentially a synthetic factory for milk. Theres nothing else like it.

During a typical 21-day course of lactation, a mouse will produce its entire body weight in lipid as well as t
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Contact: Heidi Hardman
hhardman@cell.com
617-397-2879
Cell Press
5-Dec-2006


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