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Control of amino acid uptake by the lactating mammary gland of the rat

At the peak of lactation the mammary gland of the rat removes considerable amounts of amino acids (Viiia et al., 1981). The increased demand for amino acids during this period is satisfied by an increase in dietary intake (Fell et al., 1963). As might be expected from a physiological standpoint, the major fate of amino acids taken up by the gland is the synthesis of milk proteins, but it has been observed that some are good precursors for lipid synthesis (Vifia & Williamson, 1981). We reported that pglutamyltransferase and glutathione are involved in amino acid uptake by the lactating mammary gland, thus providing evidence for the functioning of the y-glutamyl cycle in the mammary gland in uiuo (Viiia et al., 1981). We have studied the evolution of the arteriovenous differences of amino acids through the mammary gland during lactation, and found that in all cases the arteriovenous differences increase from day 0 to day 5 and from day 5 to day 10. They remain high between days 10 and 15 but fall sharply at day 20. These changes parallel those of the activity of y-glutamyltransferase in mammary gland during lactation (Puente et al., 1979). At the peak of lactation both the blood flow and the arteriovenous differences of amino acids are maximal. Thus the uptake of amino acids by the gland is maximal between days 10 and 15 after birth, when specific direction of blood metabolites to the gland is maximal (Williamson, 1980). It has been shown that y-glutamyltransferase is subject to hormonal control by oestrogens (Puente et al., 1979) and by prolactin (Pocius et al., 1980). The availability of bromocryptine, an inhibitor of prolactin secretion (Seki et al., 1974), was useful as a tool to investigate the role of prolactin in the regulation of amino acid uptake by the lactating mammary gland. We compared the arteriovenous differences through the mammary gland under the following situations: (a) normal lactating rats a t the peak of lactation; (b) rats at the peak of lactation with bromocryptine-induced prolactin deficiency (24h); and (c) rats at the peak of lactation injected with bromocryptine and prolactin. The arteriovenous differences of amino acids were significantly lower in prolactin-deficient rats than in untreated rats (P < 0.05 for threonine, serine, asparagine, cysteine, methionine, leucine, phenylalanine and lysine; P < 0.005 for glutamine, proline, glycine, alanine, isoleucine, tyrosine, hystidine and arginine). However, when prolactin was injected together with bromocryptine, as described by Agius et al . (1979), the lactating mammary gland of the rat