Horm Metab Res 2009; 41(10): 747-751
DOI: 10.1055/s-0029-1224181
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Prolactin Suppresses Malonyl-CoA Concentration in Human Adipose Tissue

L. A. Nilsson1 , C. Roepstorff2 , B. Kiens2 , H. Billig1 , C. Ling3
  • 1Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Göteborg, Sweden
  • 2The Copenhagen Muscle Research Centre, Molecular Physiology Group, Section of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, Denmark
  • 3Department of Clinical Science, Lund University Diabetes Center, CRC, Lund University, University Hospital MAS, Malmö, Sweden
Further Information

Publication History

received 08.12.2008

accepted 06.05.2009

Publication Date:
23 June 2009 (online)


Prolactin is best known for its involvement in lactation, where it regulates mechanisms that supply nutrients for milk production. In individuals with pathological hyperprolactinemia, glucose and fat homeostasis have been reported to be negatively influenced. It is not previously known, however, whether prolactin regulates lipogenesis in human adipose tissue. The aim of this study was to investigate the effect of prolactin on lipogenesis in human adipose tissue in vitro. Prolactin decreased the concentration of malonyl-CoA, the product of the first committed step in lipogenesis, to 77±6% compared to control 100±5% (p=0.022) in cultured human adipose tissue. In addition, prolactin was found to decrease glucose transporter 4 (GLUT4) mRNA expression, which may cause decreased glucose uptake. In conclusion, we propose that prolactin decreases lipogenesis in human adipose tissue as a consequence of suppressed malonyl-CoA concentration in parallel with decreased GLUT-4 expression. In the lactating woman, this regulation in adipose tissue may enhance the provision of nutrients for the infant instead of nutrients being stored in adipose tissue. In hyperprolactinemic individuals, a suppressed lipogenesis could contribute to an insulin resistant state with consequences for the health.



L. A. Nilsson

Institute of Neuroscience and Physiology

Sahlgrenska Academy at University of Gothenburg

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405 30 Göteborg


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