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Prolactin suppresses malonyl-CoA concentration in human adipose tissue

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Prolactin suppresses malonyl-CoA concentration in human adipose tissue. / Nilsson, L. A.; Roepstorff, Carsten; Kiens, Bente; Billig, H.; Ling, C.

I: Hormone and Metabolic Research, Bind 41, Nr. 10, 2009, s. 747-751.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Nilsson, LA, Roepstorff, C, Kiens, B, Billig, H & Ling, C 2009, 'Prolactin suppresses malonyl-CoA concentration in human adipose tissue', Hormone and Metabolic Research, bind 41, nr. 10, s. 747-751. https://doi.org/10.1055/s-0029-1224181

APA

Nilsson, L. A., Roepstorff, C., Kiens, B., Billig, H., & Ling, C. (2009). Prolactin suppresses malonyl-CoA concentration in human adipose tissue. Hormone and Metabolic Research, 41(10), 747-751. https://doi.org/10.1055/s-0029-1224181

Vancouver

Nilsson LA, Roepstorff C, Kiens B, Billig H, Ling C. Prolactin suppresses malonyl-CoA concentration in human adipose tissue. Hormone and Metabolic Research. 2009;41(10):747-751. https://doi.org/10.1055/s-0029-1224181

Author

Nilsson, L. A. ; Roepstorff, Carsten ; Kiens, Bente ; Billig, H. ; Ling, C. / Prolactin suppresses malonyl-CoA concentration in human adipose tissue. I: Hormone and Metabolic Research. 2009 ; Bind 41, Nr. 10. s. 747-751.

Bibtex

@article{da42af5093c411de8bc9000ea68e967b,
title = "Prolactin suppresses malonyl-CoA concentration in human adipose tissue",
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 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.",
author = "Nilsson, {L. A.} and Carsten Roepstorff and Bente Kiens and H. Billig and C. Ling",
note = "CURIS 2009 5200 107",
year = "2009",
doi = "10.1055/s-0029-1224181",
language = "English",
volume = "41",
pages = "747--751",
journal = "Hormone and Metabolic Research",
issn = "0018-5043",
publisher = "GeorgThieme Verlag",
number = "10",

}

RIS

TY - JOUR

T1 - Prolactin suppresses malonyl-CoA concentration in human adipose tissue

AU - Nilsson, L. A.

AU - Roepstorff, Carsten

AU - Kiens, Bente

AU - Billig, H.

AU - Ling, C.

N1 - CURIS 2009 5200 107

PY - 2009

Y1 - 2009

N2 - 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.

AB - 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.

U2 - 10.1055/s-0029-1224181

DO - 10.1055/s-0029-1224181

M3 - Journal article

C2 - 19551610

VL - 41

SP - 747

EP - 751

JO - Hormone and Metabolic Research

JF - Hormone and Metabolic Research

SN - 0018-5043

IS - 10

ER -

ID: 14023448