Pharmacologic inhibition of mTORC1 mimics dietary protein restriction in a mouse model of lactation.

Overall, sufficient supply of dietary amino acids was unable to maintain lactation performance status in mice with pharmacologically reduced mammary mTORC1 activity, as evidenced by diminished pup growth and milk production, supporting the concept that mTORC1 activation rather than substrate supply is the primary route by which amino acids regulate synthesis of milk components.