Target tissues respond to hormones only if specific receptors are present on or within their cells. Alterations of the hormone-receptor axis may then modify the response of target tissues (i.e., hormonal-responsive mammary carcinoma) to various hormones and serve as a means of controlling the growth and function of such tissues. We have shown that growth hormone induces the prolactin receptor in murine liver by acting at a site distal to the induced receptor. By making mice deficient in essential fatty acids, both the intraperitoneal and mammary gland fats are markedly decreased. These deficient animals lose the normal ductal-alveolar structures within their mammary glands, an effect that can be reversed by treatment with exogenous linoleic acid. These deficient animals also have decreased numbers of prolactin receptors within their livers and are unable to induce them by hormone injections. Prostaglandins have, therefore, been implicated in the maintenance and induction of the PRL receptor in vivo. These studies indicate that specific fatty acids modulate the functionality of prolactin receptors, probably by altering prostaglandin synthesis. Mammary tissues have also been shown to synthesize prostaglandins at rates that vary as a function of stage in the estrus cycle. Dietary fat may modify effects of hormones on the mammary gland.