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Prolactin reduces fat metabolism

02.04.2009
The hormone prolactin is necessary for the production of breast milk, but it also affects adipose (fatty) tissue and the body's metabolism. This has been shown by a thesis from the Sahlgrenska Academy, University of Gothenburg, Sweden. Raised prolactin levels in a woman who is not pregnant or breast feeding reduces lipid (fat) metabolism.

Over 30 000 Swedish men and women may have raised levels of prolactin. Women who are pregnant or breast feeding have naturally raised levels of prolactin, but stress, some medicines and benign brain tumours can also lead to raised levels of the hormone.

In many cases doctors don't know what causes the rise in hormone levels. In women, an abnormally high level can cause menstrual disturbances and infertility, and may also result in insulin resistance.

"In recent years scientists have also recognised the role of prolactin in the development of obesity, but little research has been done into the precise mechanism by which prolactin regulates metabolism," says Louise Nilsson.

In her thesis Louise Nilsson shows that there are receptors for the breast feeding hormone in human fatty tissue.

"We have demonstrated that prolactin reduces the ability of fatty tissue to store sugar and fat, which then could accumulate in the blood and certain tissues instead. This in turn increases the risk of cardiovascular disease."

Prolactin also affects the body's ability to metabolise fat. An ongoing study suggests that the hormone impairs the body's ability to maintain a balanced metabolism.

"When fatty tissue receives signals from prolactin, it reacts by reducing the production of another hormone called adiponectin, which is important for the metabolism of a variety of nutrients," explains Louise Nilsson.

FACTS ABOUT PROLACTIN
Prolactin is a hormone produced by the pituitary gland in the brain. It stimulates the production of milk in the breast and also inhibits hormone production in the ovaries and testicles. Prolactin levels are considerably raised in pregnancy, and prolactin secretion is also stimulated by breast feeding.

The Sahlgrenska Academy is the faculty of health sciences at the University of Gothenburg, Sweden. Education and research are conducted within the fields of pharmacy, medicine, odontology and health care sciences.

About 4000 undergraduate students and 1000 postgraduate students are enrolled at Sahlgrenska Academy. The staff is about 1500 persons. 850 of them are researchers and/or teachers.

For further information please contact:
Louise Nilsson, tel: +46 (0)31 786 3533, +46 (0)70 523 67 41, e-mail: louise.nilsson@gu.se
Supervisor:
Professor Håkan Billig, tel: +46 (0)31 786 3534, e-mail: hakan.billig@fysiologi.gu.se

Doctoral thesis from the Sahlgrenska Academy, Institute of Neuroscience and Physiology, University of Gothenburg, Sweden.

Title of thesis: Effects of prolactin on metabolism - changes induced by hyperprolactinemia

The thesis has been defended.
Link to the thesis: http://hdl.handle.net/2077/19049
Press information: Elin Lindström Claessen
Tel: +46 (0)31 786 3837, +46 (0)70 829 43 03
e-mail: elin.lindstrom@sahlgrenska.gu.se
The thesis is based on the following papers:
I Identification of functional prolactin (PRL) receptor gene expression: PRL inhibits
lipoprotein lipase activity in human white adipose tissue.
Ling C, Svensson L, Odén B, Weijdegård B, Edén B, Edén S, Billig H.
J Clin Endocrinol Metab. 2003 Apr;88(4):1804-8.
II Prolactin suppresses malonyl-CoA concentration in human adipose tissue.
Nilsson L, Roepstorff C, Kiens B, Billig H, Ling C.
Submitted
III Prolactin and growth hormone regulate adiponectin secretion and receptor
expression in adipose tissue.
Nilsson L, Binart N, Bohlooly-Y M, Bramnert M, Egecioglu E, Kindblom J, Kelly
PA, Kopchick JJ, Ormandy CJ, Ling C, Billig H.
Biochem Biophys Res Commun. 2005 Jun 17;331(4):1120-6.
IV Suppressed lipid oxidation in women with pathological hyperprolactinemia.
Nilsson L, Bramnert M, Wessman Y, Billig H, Ling C.
Manuscript

Helena Aaberg | idw
Further information:
http://hdl.handle.net/2077/19049
http://www.gu.se/

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