4.2 Article

Prolactin Suppresses Malonyl-CoA Concentration in Human Adipose Tissue

Journal

HORMONE AND METABOLIC RESEARCH
Volume 41, Issue 10, Pages 747-751

Publisher

GEORG THIEME VERLAG KG
DOI: 10.1055/s-0029-1224181

Keywords

lipogenesis; acetyl-CoA carboxylase; glucose transporter 4; retinol binding protein 4; human adipose tissue

Funding

  1. Swedish Research Council [10380, 13550, 522-2006-6480]
  2. Emil and Maria Palm Foundation
  3. Eva and Oscar Ahren Research Foundation, Stockholm
  4. Hjalmar Svensson Foundation
  5. Lars Hierta Memorial Foundation
  6. Wilhelm and Martina Lundgren Foundation
  7. European Commission [LSHM-CT-2004-005272]
  8. Knut and Alice Wallenberg Foundation
  9. Linne grant [B31 5631/2006]

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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 play 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

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