Integration of lipid metabolism in the mammary gland and adipose tissue by prolactin during lactation

  title={Integration of lipid metabolism in the mammary gland and adipose tissue by prolactin during lactation},
  author={Manuel Ros and Mar{\'i}a Fern{\'a}ndez Lobato and Josefa Predestinaci{\'o}n Garc{\'i}a-Ru{\'i}z and Francisco J. Moreno},
  journal={Molecular and Cellular Biochemistry},
Prolactin deficiency, induced by bromocryptine treatment, brought about reciprocal changes in the ability of adipocytes and acini isolated from lactating rats to synthesize lipids. The capacity to synthesize fatty acids and phospholipids decreased in the mammary gland and increased in adipocytes by bromocryptine treatment. In the mammary gland, the maximum potential activity of the pentose shunt as well as the specific activities of the pathway dehydrogenases were significantly reduced by… 

Effects of prolactin on metabolism - changes induced by hyperprolactinemia

There are indications that prolactin could be a potent and specific regulator of several metabolic processes, including the regulation of nutrient flux, which is important to maintain a balanced metabolism.

Function of phosphoenolpyruvate carboxykinase in mammary gland epithelial cells[S]

Pck1 functions in the pathway for the conversion of gluconeogenic precursors to glucose and contributes to glycerol-3-phosphate synthesis through glyceroneogenesis, and plays an important role in both the mammary gland adipocytes and epithelial cells during lactation.

The prolactin-deficient mouse has an unaltered metabolic phenotype.

It is reported that PRL deficiency does not affect the rate of weight gain, body composition, serum lipids, or adiponectin levels in either sex on any diet, and it is concluded thatPRL deficiency has negligible gross metabolic effects in mice.

Lipogenesis impaired in periparturient rats exposed to altered gravity is independent of prolactin and glucocorticoid secretion

Reduced lipogenesis in HG exposed dams is independent of PRL and GC secretion but may be associated with dysregulation of multiple metabolic regulators at the level of mRNA expression.

Adaptations of Maternal Adipose Tissue to Lactation

  • R. VernonC. Pond
  • Biology, Medicine
    Journal of Mammary Gland Biology and Neoplasia
  • 2004
Lactation results in profound changes in adipose tissue metabolism, the molecular bases of which are beginning to be resolved in domestic ruminants and laboratory rodents.

Lipidomics of mammary epithelial cells throughout differentiation

The results obtained in this work indicate that phosphatidylethanolamine (PE) show an increase in relative content with the progression to differentiation, while in the case of the other PL classes no significant changes were observed, when comparing the three types of cell.

Identification of functional prolactin (PRL) receptor gene expression: PRL inhibits lipoprotein lipase activity in human white adipose tissue.

A direct effect of PRL, via functional PRLRs, in reducing the LPL activity in human adipose tissue is demonstrated, and these results suggest that LPL might also be regulated in this fashion during lactation.


There was strong evidence supporting the hypothesis that milk lipid content is regulated at the level of mobilization of milk precursors from lipid stores, and the hormonal and enzymatic regulation of lipid mobilization exhibit differences between elephant seals and other mammals.

Conditions associated with increased growth hormone and prolactin sensitivity

The studies indicate that the tissue sensitivity to GH/PRL is regulated by SOCS2 and TSC2 proteins and to block an increased PRL sensitivity, a novel PRLRA is developed and demonstrated its efficacy in cell cultures.

What can we learn from rodents about prolactin in humans?

There is sufficient disparity in the control of the production, distribution, and physiological functions of PRL among these species to warrant careful and judicial extrapolation to humans.



Coordination of glucose metabolism and NADPH formation in the adipose tissue and mammary gland during the lactation-weaning transition.

The capacity of fat cells from 48-hour weaned mid-lactating rats to synthesize fatty acids from (1- 14C)-glucose and (6-14C)- glucose was markedly increased and the activities of the lipogenic enzymes in adipose tissue were very low during lactation but increased rapidly after weaning.

Comparison of glucose metabolism in the lactating mammary gland of the rat in vivo and in vitro. Effects of starvation, prolactin or insulin deficiency.

It is concluded that isolated acini represent a suitable model for the study of mammary-gland carbohydrate metabolism in that they reflect metabolism of the gland in vivo.

Influence of starvation/refeeding transition on lipogenesis and NADPH producing systems in adipose tissue, mammary gland and liver at mid-lactation.

All the variations observed "in vivo" and "in vitro" in mammary gland returned almost to normal values by refeeding the starved lactating rats.

Prolactin and the regulation of adipose-tissue metabolism during lactation in rats

Adenosine and the control of lipolysis in rat adipocytes during pregnancy and lactation.

The activity of 5'-nucleotidase, and hence the capacity of the cells to synthesize adenosine, was the same in fat-cells and also stromal cells of adipose tissue from pregnant, lactating and male rats.

Primary role of decreased fatty acid synthesis in insulin resistance of large rat adipocytes.

The data provide strong support for the hypothesis that the fatty acid synthetic pathway is the primary metabolic defect in large insulin-resistant rat adipocytes, a defect which secondarily leads to inhibited pentose shunt activity.

Integration of metabolism in tissues of the lactating rat

Lipogenesis by acini from mammary gland of lactating rats.

Regulation of acetyl-CoA carboxylase in rat mammary gland. Effects of starvation and of insulin and prolactin deficiency on the fraction of the enzyme in the active form in vivo.

It is suggested that acetyl-CoA carboxylase activity is rate-limiting for lipogenesis in the mammary gland in normal, fed, suckled or weaned animals but that in starved and short-term diabetic animals changes in the activity of the enzyme by covalent modification alone may not be sufficient to maintain the enzyme in its rate- Limiting role.

The mode of regulation of pyruvate dehydrogenase of lactating rat mammary gland. Effects of starvation and insulin.

Changes in activity of the intrinsic kinase and phosphatase of the pyruvate dehydrogenase complex of lactating rat mammary gland are not explicable by current theories of regulation of the complex.