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Pituitary. 2008 Mar 13. [Epub ahead of print]
The effects of hyperprolactinemia on bone and fat.
Shibli-Rahhal A, Schlechte J.
Department of Internal Medicine, University of Iowa Hospitals and
Clinics, Iowa City, IA, 52242, USA.
Many patients with prolactin secreting pituitary tumors have decreased
bone mineral. The bone loss is associated with an increase in bone
resorption and is secondary to prolactin-induced hypogonadism. In both
sexes trabecular bone in the spine and hip is more affected than
cortical bone in the distal radius. Normalization of prolactin and
restoration of gonadal function increases bone density but is not
associated with normalization of bone mass. It is not known whether
the bone loss in hyperprolactinemic subjects represents a failure to
achieve peak bone mass or is due to accelerated bone loss. Despite low
bone density hyperprolactinemic subjects do not demonstrate increased
fractures. The association between prolactin, weight gain and obesity
suggests that prolactin may also be a modulator of body composition
and body weight. It is not known whether hyperprolactinemia associated
weight gain is due to stimulation of lipogenesis or due to disruption
of central nervous system dopaminergic tone. Hyperprolactinemia is
also associated with
insulin resistance and endothelial dysfunction
which may improve after normalization of prolactin. The clinical
significance of these findings and the precise role of prolactin in
regulation of weight and metabolism remain to be elucidated.
PMID: 18338266
Diabetes Obes Metab. 2007 Jul;9(4):464-76.
Adipocyte prolactin: regulation of release and putative functions.
Brandebourg T, Hugo E, Ben-Jonathan N.
Department of Cell Biology, University of Cincinnati School of
Medicine, Cincinnati, OH, USA.
Pituitary-derived prolactin (PRL) is a well-known regulator of the
lactating mammary gland. However, the recent discovery that human
adipose tissue produces PRL as well as expresses the PRL receptor
(PRLR) highlights a previously unappreciated action of PRL as a
cytokine involved in adipose tissue function. Biologically active PRL
is secreted by all adipose tissue depots examined: breast, visceral
and subcutaneous. The expression of adipose PRL is regulated by a non-
pituitary, alternative superdistal promoter. PRL expression and
release increases during early pre-adipocyte differentiation and is
stimulated by cyclic AMP activators, including beta adrenergic
receptor agonists. PRL release from subcutaneous adipose explants is
attenuated during obesity, suggesting that adipose PRL production is
altered by the metabolic state. Several lines of evidence indicate
that PRL suppresses lipid storage as well as the release of adipokines
such as adiponectin, interleukin-6 and possibly leptin. PRL has also
been implicated in the regulation of adipogenesis. A newly developed
PRL-secreting human adipocyte cell line, LS14, should allow
comprehensive examination of the regulation and function of adipocyte-
derived PRL. Collectively, these studies raise the prospect that PRL
affects energy homeostasis through its action as an adipokine and is
involved in the manifestation of insulin resistance.
PMID: 17587388