Steen Bønløkke Pedersen

Gene Expression in Skeletal Muscle after an Acute Intravenous GH Bolus in Human Subjects: Identification of a Mechanism Regulating ANGPTL4

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Gene Expression in Skeletal Muscle after an Acute Intravenous GH Bolus in Human Subjects: Identification of a Mechanism Regulating ANGPTL4. / Clasen, Berthil F F; Hafstrøm, Thomas Krusenstjerna-; Vendelbo, Mikkel Holm; Thorsen, Kasper; Escande, Carlos; Moller, Niels; Pedersen, Steen B; Jørgensen, Jens Otto Lunde; Jessen, Niels.

I: Journal of Lipid Research, Bind 54, Nr. 7, 20.07.2013, s. 1988-1997.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

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@article{01d7c621fdf64330a264a63c72143567,
title = "Gene Expression in Skeletal Muscle after an Acute Intravenous GH Bolus in Human Subjects: Identification of a Mechanism Regulating ANGPTL4",
abstract = "Growth hormone (GH) acutely stimulates lipolysis and fat oxidation, a process which operates postabsorptively and involves activation of the JAK-STAT pathway in the target tissue; no in vivo data exist regarding subsequent GH-regulated gene transcription. We obtained serum samples and muscle biopsies in human subjects before and 2 h after administration of a GH bolus. A significant 75 % elevation in serum FFA levels was recorded post GH. Microarray identified 79 GH-regulated genes in muscle. With qRT-PCR we then examined the expression of selected genes in the presence and absence of glucose-induced suppression of lipolysis. Four genes involved in the JAK-STAT5 signaling pathway were regulated by GH, including SOCS1-3 and CISH, in addition to three genes associated with insulin action: NFkB1A, PIK3C2B, and PRKAG2. The gene encoding ANGPTL4, a protein involved in lipolysis and suppression of LPL activity, exhibited the most pronounced up regulation (5.6 fold) after GH, which was abrogated by concomitant suppression of lipolysis. The GH-induced stimulation of ANGPTL4 gene expression therefore seems secondary to induction of lipolysis. This new concept would imply that abundant supply of circulating FFA would decrease the need for alternative triglyceride derived FFA through distinct inhibition of LPL mediated by increased ANGPTL4 gene expression in human muscle.",
author = "Clasen, {Berthil F F} and Hafstr{\o}m, {Thomas Krusenstjerna-} and Vendelbo, {Mikkel Holm} and Kasper Thorsen and Carlos Escande and Niels Moller and Pedersen, {Steen B} and J{\o}rgensen, {Jens Otto Lunde} and Niels Jessen",
year = "2013",
month = jul,
day = "20",
doi = "10.1194/jlr.P034520",
language = "English",
volume = "54",
pages = "1988--1997",
journal = "Journal of Lipid Research",
issn = "0022-2275",
publisher = "American Society for Biochemistry and Molecular Biology, Inc.",
number = "7",

}

RIS

TY - JOUR

T1 - Gene Expression in Skeletal Muscle after an Acute Intravenous GH Bolus in Human Subjects: Identification of a Mechanism Regulating ANGPTL4

AU - Clasen, Berthil F F

AU - Hafstrøm, Thomas Krusenstjerna-

AU - Vendelbo, Mikkel Holm

AU - Thorsen, Kasper

AU - Escande, Carlos

AU - Moller, Niels

AU - Pedersen, Steen B

AU - Jørgensen, Jens Otto Lunde

AU - Jessen, Niels

PY - 2013/7/20

Y1 - 2013/7/20

N2 - Growth hormone (GH) acutely stimulates lipolysis and fat oxidation, a process which operates postabsorptively and involves activation of the JAK-STAT pathway in the target tissue; no in vivo data exist regarding subsequent GH-regulated gene transcription. We obtained serum samples and muscle biopsies in human subjects before and 2 h after administration of a GH bolus. A significant 75 % elevation in serum FFA levels was recorded post GH. Microarray identified 79 GH-regulated genes in muscle. With qRT-PCR we then examined the expression of selected genes in the presence and absence of glucose-induced suppression of lipolysis. Four genes involved in the JAK-STAT5 signaling pathway were regulated by GH, including SOCS1-3 and CISH, in addition to three genes associated with insulin action: NFkB1A, PIK3C2B, and PRKAG2. The gene encoding ANGPTL4, a protein involved in lipolysis and suppression of LPL activity, exhibited the most pronounced up regulation (5.6 fold) after GH, which was abrogated by concomitant suppression of lipolysis. The GH-induced stimulation of ANGPTL4 gene expression therefore seems secondary to induction of lipolysis. This new concept would imply that abundant supply of circulating FFA would decrease the need for alternative triglyceride derived FFA through distinct inhibition of LPL mediated by increased ANGPTL4 gene expression in human muscle.

AB - Growth hormone (GH) acutely stimulates lipolysis and fat oxidation, a process which operates postabsorptively and involves activation of the JAK-STAT pathway in the target tissue; no in vivo data exist regarding subsequent GH-regulated gene transcription. We obtained serum samples and muscle biopsies in human subjects before and 2 h after administration of a GH bolus. A significant 75 % elevation in serum FFA levels was recorded post GH. Microarray identified 79 GH-regulated genes in muscle. With qRT-PCR we then examined the expression of selected genes in the presence and absence of glucose-induced suppression of lipolysis. Four genes involved in the JAK-STAT5 signaling pathway were regulated by GH, including SOCS1-3 and CISH, in addition to three genes associated with insulin action: NFkB1A, PIK3C2B, and PRKAG2. The gene encoding ANGPTL4, a protein involved in lipolysis and suppression of LPL activity, exhibited the most pronounced up regulation (5.6 fold) after GH, which was abrogated by concomitant suppression of lipolysis. The GH-induced stimulation of ANGPTL4 gene expression therefore seems secondary to induction of lipolysis. This new concept would imply that abundant supply of circulating FFA would decrease the need for alternative triglyceride derived FFA through distinct inhibition of LPL mediated by increased ANGPTL4 gene expression in human muscle.

U2 - 10.1194/jlr.P034520

DO - 10.1194/jlr.P034520

M3 - Journal article

C2 - 23606725

VL - 54

SP - 1988

EP - 1997

JO - Journal of Lipid Research

JF - Journal of Lipid Research

SN - 0022-2275

IS - 7

ER -