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Prolactin Suppresses Malonyl-CoA Concentration in Human Adipose Tissue

Nilsson, L. A.; Roepstorff, C.; Kiens, B.; Billig, H. and Ling, Charlotte LU (2009) In Hormone and Metabolic Research 41(10). p.747-751
Abstract
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... (More)
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 (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
retinol, glucose transporter 4, lipogenesis, acetyl-CoA carboxylase, binding protein 4, human adipose tissue
in
Hormone and Metabolic Research
volume
41
issue
10
pages
747 - 751
publisher
Georg Thieme Verlag
external identifiers
  • wos:000271420500005
  • scopus:70350380094
ISSN
1439-4286
DOI
10.1055/s-0029-1224181
language
English
LU publication?
yes
id
726bc149-01df-4f96-a692-058707b1d31a (old id 1520202)
date added to LUP
2009-12-28 10:13:14
date last changed
2017-01-08 04:50:07
@article{726bc149-01df-4f96-a692-058707b1d31a,
  abstract     = {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},
  author       = {Nilsson, L. A. and Roepstorff, C. and Kiens, B. and Billig, H. and Ling, Charlotte},
  issn         = {1439-4286},
  keyword      = {retinol,glucose transporter 4,lipogenesis,acetyl-CoA carboxylase,binding protein 4,human adipose tissue},
  language     = {eng},
  number       = {10},
  pages        = {747--751},
  publisher    = {Georg Thieme Verlag},
  series       = {Hormone and Metabolic Research},
  title        = {Prolactin Suppresses Malonyl-CoA Concentration in Human Adipose Tissue},
  url          = {http://dx.doi.org/10.1055/s-0029-1224181},
  volume       = {41},
  year         = {2009},
}