Endocrine Abstracts

Today prolactin (PRL) has been demonstrated to regulate more then 300 different biological functions, including metabolism during lactation and in subjects with hyperprolactinemia. However, the mechanisms for how PRL regulates the adipose tissue in humans and rodents have remained unclear. We recently reported PRL receptor (PRLR) expression in the adipose tissue of lactating and in PRL-transgenic mice. These results suggest PRLR-mediated effects in adipose tissue. However, to date most studies have been performed in vivo, and it is unclear whether PRL has direct effects on adipocytes. The PRLR belongs to the cytokine receptor family, and a family of suppressors of cytokine signaling (SOCS) has been identified. We recently demonstrated that PRL induced CIS mRNA and a combination of PRL and insulin induced the expression of SOCS-3 in cultured adipocytes. In vivo, PRL transiently induces the expression of CIS, SOCS-2 and SOCS-3 in female mice. However, in PRL transgenic mice with chronic high PRL levels only SOCS-2 expression was elevated. PRL also stimulated leptin production in vitro. It is known that during lactation serum levels of PRL are elevated and the activity of lipoprotein lipase (LPL) is decreased in the adipose tissue and increased in the mammary gland. However, PRL has been suggested to affect the adipose tissue in an indirect fashion during lactation. In recent studies we have demonstrated the expression of four PRLR mRNA forms (L-, I-, SIa- and Slb-) in human subcutaneous abdominal adipose tissue and breast adipose tissue. We have also demonstrated that PRLR in human adipose tissue is functional. PRL reduced the LPL activity in human adipose tissue in vitro and inhibited cortisol-induced LPL activity.
The demonstration of functional PRLR in human and rodent white adipose tissue opens the possibility for PRL to be an important physiological regulator of adipose metabolism during pregnancy and lactation.