The role of growth hormone, prolactin and insulin-like growth factors in the regulation of rat mammary gland and adipose tissue metabolism during lactation

Abstract

ABSTRACT Inhibition of prolactin secretion with bromocriptine and neutralization of GH action with a specific antiserum to rat GH (rGH) were used to explore the modes of action of GH and prolactin in maintaining lactation in the rat. Treatment of dams with anti-rGH caused a small reduction in litter weight gain whilst bromocriptine reduced litter weight gain by 50%. When both treatments were combined, however, milk yield ceased completely and this wasaccompanied by a wide variety of effects on mammary lipid metabolism including decreases in the mRNA concentrations of acetyl CoA carboxylase, fatty acid synthase, malic enzyme and lipoprotein lipase. Activities of acetyl CoA carboxylase and lipoprotein lipase were also significantly reduced. Reciprocal changes were evident in adipose tissue with increases in acetyl CoA carboxylase and lipoprotein lipase activities. In conjunction with a decreased lipolytic response to noradrenaline in adipose tissue of animals given the combined treatment of bromocriptine and anti-rGH, this represented a co-ordinated series of changes to reduce lipid synthesis in the mammary gland and enhance lipogenesis and triglyceride storage in adipose tissue as milk production ceased. All of these effects could be prevented in part by concurrent treatment with GH, but insulin-like growth factor-I (IGF-I) and IGF-II failed to affect any of the parameters measured. Taken as a whole, these data suggest that (1) both prolactin and GH induce a co-ordinated series of changes in the mammary gland, (2) the intracellular controls involved clearly operate at the level of gene transcription although post-translational controls are also probably involved, (3) the effects of GH on the mammary gland could not be mimicked by IGFs and (4) although GH clearly regulates lipid metabolism in adipose tissue in a manner which should favour nutrient utilization by the mammary gland, these effects are probably too small to account for the effects of GH on milk production. Since GH receptors have not been reported to be present on mammary secretory cells, the precise mode of action of GH remains uncertain. Journal of Endocrinology (1992) 135, 195–202