SOCS-1 deficiency does not prevent diet-induced insulin resistance

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SOCS-1 deficiency does not prevent diet-induced insulin resistance. / Emanuelli, Brice; Macotela, Yazmin; Boucher, Jérémie; Ronald Kahn, C.

In: Biochemical and Biophysical Research Communications, Vol. 377, No. 2, 12.12.2008, p. 447-52.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Emanuelli, B, Macotela, Y, Boucher, J & Ronald Kahn, C 2008, 'SOCS-1 deficiency does not prevent diet-induced insulin resistance', Biochemical and Biophysical Research Communications, vol. 377, no. 2, pp. 447-52. https://doi.org/10.1016/j.bbrc.2008.09.158

APA

Emanuelli, B., Macotela, Y., Boucher, J., & Ronald Kahn, C. (2008). SOCS-1 deficiency does not prevent diet-induced insulin resistance. Biochemical and Biophysical Research Communications, 377(2), 447-52. https://doi.org/10.1016/j.bbrc.2008.09.158

Vancouver

Emanuelli B, Macotela Y, Boucher J, Ronald Kahn C. SOCS-1 deficiency does not prevent diet-induced insulin resistance. Biochemical and Biophysical Research Communications. 2008 Dec 12;377(2):447-52. https://doi.org/10.1016/j.bbrc.2008.09.158

Author

Emanuelli, Brice ; Macotela, Yazmin ; Boucher, Jérémie ; Ronald Kahn, C. / SOCS-1 deficiency does not prevent diet-induced insulin resistance. In: Biochemical and Biophysical Research Communications. 2008 ; Vol. 377, No. 2. pp. 447-52.

Bibtex

@article{6b6ab3481c75480dbbebe2692dae8146,
title = "SOCS-1 deficiency does not prevent diet-induced insulin resistance",
abstract = "Obesity is associated with inflammation and increased expression of suppressor of cytokine signaling (SOCS) proteins, which inhibit cytokine and insulin signaling. Thus, reducing SOCS expression could prevent the development of obesity-induced insulin resistance. Using SOCS-1 knockout mice, we investigated the contribution of SOCS-1 in the development of insulin resistance induced by a high-fat diet (HFD). SOCS-1 knockout mice on HFD gained 70% more weight, displayed a 2.3-fold increase in epididymal fat pads mass and increased hepatic lipid content. This was accompanied by increased mRNA expression of leptin and the macrophage marker CD68 in white adipose tissue and of SREBP1c and FAS in liver. HFD also induced hyperglycemia in SOCS-1 deficient mice with impairment of glucose and insulin tolerance tests. Thus, despite the role of SOCS proteins in obesity-related insulin resistance, SOCS-1 deficiency alone is not able to prevent insulin resistance induced by a diet rich in fat.",
keywords = "Animals, DNA-Binding Proteins, Diet, Dietary Fats, Fatty Liver, Gene Expression, Insulin Resistance, Mice, Mice, Knockout, Obesity, Suppressor of Cytokine Signaling Proteins",
author = "Brice Emanuelli and Yazmin Macotela and J{\'e}r{\'e}mie Boucher and {Ronald Kahn}, C",
year = "2008",
month = dec,
day = "12",
doi = "10.1016/j.bbrc.2008.09.158",
language = "English",
volume = "377",
pages = "447--52",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Elsevier",
number = "2",

}

RIS

TY - JOUR

T1 - SOCS-1 deficiency does not prevent diet-induced insulin resistance

AU - Emanuelli, Brice

AU - Macotela, Yazmin

AU - Boucher, Jérémie

AU - Ronald Kahn, C

PY - 2008/12/12

Y1 - 2008/12/12

N2 - Obesity is associated with inflammation and increased expression of suppressor of cytokine signaling (SOCS) proteins, which inhibit cytokine and insulin signaling. Thus, reducing SOCS expression could prevent the development of obesity-induced insulin resistance. Using SOCS-1 knockout mice, we investigated the contribution of SOCS-1 in the development of insulin resistance induced by a high-fat diet (HFD). SOCS-1 knockout mice on HFD gained 70% more weight, displayed a 2.3-fold increase in epididymal fat pads mass and increased hepatic lipid content. This was accompanied by increased mRNA expression of leptin and the macrophage marker CD68 in white adipose tissue and of SREBP1c and FAS in liver. HFD also induced hyperglycemia in SOCS-1 deficient mice with impairment of glucose and insulin tolerance tests. Thus, despite the role of SOCS proteins in obesity-related insulin resistance, SOCS-1 deficiency alone is not able to prevent insulin resistance induced by a diet rich in fat.

AB - Obesity is associated with inflammation and increased expression of suppressor of cytokine signaling (SOCS) proteins, which inhibit cytokine and insulin signaling. Thus, reducing SOCS expression could prevent the development of obesity-induced insulin resistance. Using SOCS-1 knockout mice, we investigated the contribution of SOCS-1 in the development of insulin resistance induced by a high-fat diet (HFD). SOCS-1 knockout mice on HFD gained 70% more weight, displayed a 2.3-fold increase in epididymal fat pads mass and increased hepatic lipid content. This was accompanied by increased mRNA expression of leptin and the macrophage marker CD68 in white adipose tissue and of SREBP1c and FAS in liver. HFD also induced hyperglycemia in SOCS-1 deficient mice with impairment of glucose and insulin tolerance tests. Thus, despite the role of SOCS proteins in obesity-related insulin resistance, SOCS-1 deficiency alone is not able to prevent insulin resistance induced by a diet rich in fat.

KW - Animals

KW - DNA-Binding Proteins

KW - Diet

KW - Dietary Fats

KW - Fatty Liver

KW - Gene Expression

KW - Insulin Resistance

KW - Mice

KW - Mice, Knockout

KW - Obesity

KW - Suppressor of Cytokine Signaling Proteins

U2 - 10.1016/j.bbrc.2008.09.158

DO - 10.1016/j.bbrc.2008.09.158

M3 - Journal article

C2 - 18929539

VL - 377

SP - 447

EP - 452

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 2

ER -

ID: 143328590