Earlier studies by the researchers found that the protein kinase Akt1 rises in concentration during pregnancy and lactation, suggesting a potential developmental role for the kinase in milk production. Another study showed that permanent activation of Akt1 in the mammary glands of mice leads to early lipid accumulation during pregnancy, raising the possibility that the gene might be important in the increased synthetic demand for lipid during lactation.
To further investigate, in the current study, the researchers examined mice lacking either Akt1 or the related gene Akt2, which are expressed in the same areas of the mammary gland at distinct developmental stages. While Akt1 protein increases during pregnancy and lactation, Akt2 levels decline.
Indeed, the researchers found that the mammary gland cells of Akt1-deficient mice failed to engage critical metabolic pathways during the transition from pregnancy to lactation, which in turn led to other deficiencies. Specifically, the mammary cells failed to increase their uptake of glucose, cells?primary energy source, and their synthesis of lipid. The cells also did not lower the level of enzymes that break down lipids.
As early as two days after birth, pups nursed by mice lacking Akt1 weighed significantly less than those nursed by normal mothers. That difference in weight only grew more exaggerated with time. In contrast, the researchers reported,