Transgenic Rescue of Adipocyte Glucose-dependent Insulinotropic Polypeptide Receptor Expression Restores High Fat Diet-induced Body Weight Gain

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Standard

Transgenic Rescue of Adipocyte Glucose-dependent Insulinotropic Polypeptide Receptor Expression Restores High Fat Diet-induced Body Weight Gain. / Ugleholdt, Randi; Pedersen, Jens; Bassi, Maria Rosaria; Füchtbauer, Ernst-Martin; Jørgensen, Signe Marie; Kissow, Hanne-Louise; Nytofte, Nikolaj; Poulsen, Steen Seier; Rosenkilde, Mette Marie; Seino, Yutaka; Thams, Peter; Holst, Peter Johannes ; Holst, Jens Juul.

I: Journal of Biological Chemistry, Bind 286, Nr. 52, 30.12.2011, s. 44632-44645.

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

Harvard

Ugleholdt, R, Pedersen, J, Bassi, MR, Füchtbauer, E-M, Jørgensen, SM, Kissow, H-L, Nytofte, N, Poulsen, SS, Rosenkilde, MM, Seino, Y, Thams, P, Holst, PJ & Holst, JJ 2011, 'Transgenic Rescue of Adipocyte Glucose-dependent Insulinotropic Polypeptide Receptor Expression Restores High Fat Diet-induced Body Weight Gain', Journal of Biological Chemistry, bind 286, nr. 52, s. 44632-44645. https://doi.org/10.1074/jbc.M111.311779

APA

Ugleholdt, R., Pedersen, J., Bassi, M. R., Füchtbauer, E-M., Jørgensen, S. M., Kissow, H-L., ... Holst, J. J. (2011). Transgenic Rescue of Adipocyte Glucose-dependent Insulinotropic Polypeptide Receptor Expression Restores High Fat Diet-induced Body Weight Gain. Journal of Biological Chemistry, 286(52), 44632-44645. https://doi.org/10.1074/jbc.M111.311779

CBE

Ugleholdt R, Pedersen J, Bassi MR, Füchtbauer E-M, Jørgensen SM, Kissow H-L, Nytofte N, Poulsen SS, Rosenkilde MM, Seino Y, Thams P, Holst PJ, Holst JJ. 2011. Transgenic Rescue of Adipocyte Glucose-dependent Insulinotropic Polypeptide Receptor Expression Restores High Fat Diet-induced Body Weight Gain. Journal of Biological Chemistry. 286(52):44632-44645. https://doi.org/10.1074/jbc.M111.311779

MLA

Vancouver

Ugleholdt R, Pedersen J, Bassi MR, Füchtbauer E-M, Jørgensen SM, Kissow H-L o.a. Transgenic Rescue of Adipocyte Glucose-dependent Insulinotropic Polypeptide Receptor Expression Restores High Fat Diet-induced Body Weight Gain. Journal of Biological Chemistry. 2011 dec 30;286(52):44632-44645. https://doi.org/10.1074/jbc.M111.311779

Author

Ugleholdt, Randi ; Pedersen, Jens ; Bassi, Maria Rosaria ; Füchtbauer, Ernst-Martin ; Jørgensen, Signe Marie ; Kissow, Hanne-Louise ; Nytofte, Nikolaj ; Poulsen, Steen Seier ; Rosenkilde, Mette Marie ; Seino, Yutaka ; Thams, Peter ; Holst, Peter Johannes ; Holst, Jens Juul. / Transgenic Rescue of Adipocyte Glucose-dependent Insulinotropic Polypeptide Receptor Expression Restores High Fat Diet-induced Body Weight Gain. I: Journal of Biological Chemistry. 2011 ; Bind 286, Nr. 52. s. 44632-44645.

Bibtex

@article{3b9925266be94f38ba7e4b2ea956b13d,
title = "Transgenic Rescue of Adipocyte Glucose-dependent Insulinotropic Polypeptide Receptor Expression Restores High Fat Diet-induced Body Weight Gain",
abstract = "The glucose-dependent insulinotropic polypeptide receptor (GIPr) has been implicated in high fat diet-induced obesity and is proposed as an anti-obesity target despite an uncertainty regarding the mechanism of action. To independently investigate the contribution of the insulinotropic effects and the direct effects on adipose tissue, we generated transgenic mice with targeted expression of the human GIPr to white adipose tissue or beta-cells, respectively. These mice were then cross-bred with the GIPr knock-out strain. The central findings of the study are that mice with GIPr expression targeted to adipose tissue have a similar high fat diet -induced body weight gain as control mice, significantly greater than the weight gain in mice with a general ablation of the receptor. Surprisingly, this difference was due to an increase in total lean body mass rather than a gain in total fat mass that was similar between the groups. In contrast, glucose-dependent insulinotropic polypeptide-mediated insulin secretion does not seem to be important for regulation of body weight after high fat feeding. The study supports a role of the adipocyte GIPr in nutrient-dependent regulation of body weight and lean mass, but it does not support a direct and independent role for the adipocyte or beta-cell GIPr in promoting adipogenesis.",
author = "Randi Ugleholdt and Jens Pedersen and Bassi, {Maria Rosaria} and Ernst-Martin F{\"u}chtbauer and J{\o}rgensen, {Signe Marie} and Hanne-Louise Kissow and Nikolaj Nytofte and Poulsen, {Steen Seier} and Rosenkilde, {Mette Marie} and Yutaka Seino and Peter Thams and Holst, {Peter Johannes} and Holst, {Jens Juul}",
year = "2011",
month = "12",
day = "30",
doi = "10.1074/jbc.M111.311779",
language = "English",
volume = "286",
pages = "44632--44645",
journal = "Journal of Biological Chemistry",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology, Inc.",
number = "52",

}

RIS

TY - JOUR

T1 - Transgenic Rescue of Adipocyte Glucose-dependent Insulinotropic Polypeptide Receptor Expression Restores High Fat Diet-induced Body Weight Gain

AU - Ugleholdt, Randi

AU - Pedersen, Jens

AU - Bassi, Maria Rosaria

AU - Füchtbauer, Ernst-Martin

AU - Jørgensen, Signe Marie

AU - Kissow, Hanne-Louise

AU - Nytofte, Nikolaj

AU - Poulsen, Steen Seier

AU - Rosenkilde, Mette Marie

AU - Seino, Yutaka

AU - Thams, Peter

AU - Holst, Peter Johannes

AU - Holst, Jens Juul

PY - 2011/12/30

Y1 - 2011/12/30

N2 - The glucose-dependent insulinotropic polypeptide receptor (GIPr) has been implicated in high fat diet-induced obesity and is proposed as an anti-obesity target despite an uncertainty regarding the mechanism of action. To independently investigate the contribution of the insulinotropic effects and the direct effects on adipose tissue, we generated transgenic mice with targeted expression of the human GIPr to white adipose tissue or beta-cells, respectively. These mice were then cross-bred with the GIPr knock-out strain. The central findings of the study are that mice with GIPr expression targeted to adipose tissue have a similar high fat diet -induced body weight gain as control mice, significantly greater than the weight gain in mice with a general ablation of the receptor. Surprisingly, this difference was due to an increase in total lean body mass rather than a gain in total fat mass that was similar between the groups. In contrast, glucose-dependent insulinotropic polypeptide-mediated insulin secretion does not seem to be important for regulation of body weight after high fat feeding. The study supports a role of the adipocyte GIPr in nutrient-dependent regulation of body weight and lean mass, but it does not support a direct and independent role for the adipocyte or beta-cell GIPr in promoting adipogenesis.

AB - The glucose-dependent insulinotropic polypeptide receptor (GIPr) has been implicated in high fat diet-induced obesity and is proposed as an anti-obesity target despite an uncertainty regarding the mechanism of action. To independently investigate the contribution of the insulinotropic effects and the direct effects on adipose tissue, we generated transgenic mice with targeted expression of the human GIPr to white adipose tissue or beta-cells, respectively. These mice were then cross-bred with the GIPr knock-out strain. The central findings of the study are that mice with GIPr expression targeted to adipose tissue have a similar high fat diet -induced body weight gain as control mice, significantly greater than the weight gain in mice with a general ablation of the receptor. Surprisingly, this difference was due to an increase in total lean body mass rather than a gain in total fat mass that was similar between the groups. In contrast, glucose-dependent insulinotropic polypeptide-mediated insulin secretion does not seem to be important for regulation of body weight after high fat feeding. The study supports a role of the adipocyte GIPr in nutrient-dependent regulation of body weight and lean mass, but it does not support a direct and independent role for the adipocyte or beta-cell GIPr in promoting adipogenesis.

U2 - 10.1074/jbc.M111.311779

DO - 10.1074/jbc.M111.311779

M3 - Journal article

VL - 286

SP - 44632

EP - 44645

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

SN - 0021-9258

IS - 52

ER -