The nitroxide radical TEMPOL prevents obesity, hyperlipidaemia, elevation of inflammatory cytokines, and modulates atherosclerotic plaque composition in apoE(-/-) mice

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The nitroxide radical TEMPOL prevents obesity, hyperlipidaemia, elevation of inflammatory cytokines, and modulates atherosclerotic plaque composition in apoE(-/-) mice. / Kim, Christine H. J.; Mitchell, James B.; Bursill, Christina A.; Sowers, Anastasia L.; Thetford, Angela; Cook, John A.; van Reyk, David M.; Davies, Michael J.

In: Atherosclerosis, Vol. 240, No. 1, 05.2015, p. 234-241.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Kim, CHJ, Mitchell, JB, Bursill, CA, Sowers, AL, Thetford, A, Cook, JA, van Reyk, DM & Davies, MJ 2015, 'The nitroxide radical TEMPOL prevents obesity, hyperlipidaemia, elevation of inflammatory cytokines, and modulates atherosclerotic plaque composition in apoE(-/-) mice', Atherosclerosis, vol. 240, no. 1, pp. 234-241. https://doi.org/10.1016/j.atherosclerosis.2015.03.012

APA

Kim, C. H. J., Mitchell, J. B., Bursill, C. A., Sowers, A. L., Thetford, A., Cook, J. A., van Reyk, D. M., & Davies, M. J. (2015). The nitroxide radical TEMPOL prevents obesity, hyperlipidaemia, elevation of inflammatory cytokines, and modulates atherosclerotic plaque composition in apoE(-/-) mice. Atherosclerosis, 240(1), 234-241. https://doi.org/10.1016/j.atherosclerosis.2015.03.012

Vancouver

Kim CHJ, Mitchell JB, Bursill CA, Sowers AL, Thetford A, Cook JA et al. The nitroxide radical TEMPOL prevents obesity, hyperlipidaemia, elevation of inflammatory cytokines, and modulates atherosclerotic plaque composition in apoE(-/-) mice. Atherosclerosis. 2015 May;240(1):234-241. https://doi.org/10.1016/j.atherosclerosis.2015.03.012

Author

Kim, Christine H. J. ; Mitchell, James B. ; Bursill, Christina A. ; Sowers, Anastasia L. ; Thetford, Angela ; Cook, John A. ; van Reyk, David M. ; Davies, Michael J. / The nitroxide radical TEMPOL prevents obesity, hyperlipidaemia, elevation of inflammatory cytokines, and modulates atherosclerotic plaque composition in apoE(-/-) mice. In: Atherosclerosis. 2015 ; Vol. 240, No. 1. pp. 234-241.

Bibtex

@article{7051f48d3fb747cfaaf0aad886cbc23a,
title = "The nitroxide radical TEMPOL prevents obesity, hyperlipidaemia, elevation of inflammatory cytokines, and modulates atherosclerotic plaque composition in apoE(-/-) mice",
abstract = "OBJECTIVE: The nitroxide compound TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl radical) has been shown to prevent obesity-induced changes in adipokines in cell and animal systems. In this study we investigated whether supplementation with TEMPOL inhibits inflammation and atherosclerosis in apoE(-/-) mice fed a high fat diet (HFD).METHODS: ApoE(-/-) mice were fed for 12 weeks on standard chow diet or a high-fat diet. Half the mice were supplemented with 10 mg/g TEMPOL in their food. Plasma samples were analysed for triglycerides, cholesterol, low- and high-density lipoprotein cholesterol, inflammatory cytokines and markers (interleukin-6, IL-6; monocyte-chemotactic protein, MCP-1; myeloperoxidase, MPO; serum amyloid A, SAA; adiponectin; leptin). Plaques in the aortic sinus were analysed for area, and content of collagen, lipid, macrophages and smooth muscle cells.RESULTS: High fat feeding resulted in marked increases in body mass and plasma lipid levels. Dietary TEMPOL decreased both parameters. In the high-fat-fed mice significant elevations in plasma lipid levels and the inflammatory markers IL-6, MCP-1, MPO, SAA were detected, along with an increase in leptin and a decrease in adiponectin. TEMPOL supplementation reversed these effects. When compared to HFD-fed mice, TEMPOL supplementation increased plaque collagen content, decreased lipid content and increased macrophage numbers.CONCLUSIONS: These data indicate that in a well-established model of obesity-associated hyperlipidaemia and atherosclerosis, TEMPOL had a significant impact on body mass, atherosclerosis, hyperlipidaemia and inflammation. TEMPOL may therefore be of value in suppressing obesity, metabolic disorders and increasing atherosclerotic plaque stability.",
author = "Kim, {Christine H. J.} and Mitchell, {James B.} and Bursill, {Christina A.} and Sowers, {Anastasia L.} and Angela Thetford and Cook, {John A.} and {van Reyk}, {David M.} and Davies, {Michael J.}",
note = "Copyright {\textcopyright} 2015 Elsevier Ireland Ltd. All rights reserved.",
year = "2015",
month = may,
doi = "10.1016/j.atherosclerosis.2015.03.012",
language = "English",
volume = "240",
pages = "234--241",
journal = "Atherosclerosis",
issn = "0021-9150",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

RIS

TY - JOUR

T1 - The nitroxide radical TEMPOL prevents obesity, hyperlipidaemia, elevation of inflammatory cytokines, and modulates atherosclerotic plaque composition in apoE(-/-) mice

AU - Kim, Christine H. J.

AU - Mitchell, James B.

AU - Bursill, Christina A.

AU - Sowers, Anastasia L.

AU - Thetford, Angela

AU - Cook, John A.

AU - van Reyk, David M.

AU - Davies, Michael J.

N1 - Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

PY - 2015/5

Y1 - 2015/5

N2 - OBJECTIVE: The nitroxide compound TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl radical) has been shown to prevent obesity-induced changes in adipokines in cell and animal systems. In this study we investigated whether supplementation with TEMPOL inhibits inflammation and atherosclerosis in apoE(-/-) mice fed a high fat diet (HFD).METHODS: ApoE(-/-) mice were fed for 12 weeks on standard chow diet or a high-fat diet. Half the mice were supplemented with 10 mg/g TEMPOL in their food. Plasma samples were analysed for triglycerides, cholesterol, low- and high-density lipoprotein cholesterol, inflammatory cytokines and markers (interleukin-6, IL-6; monocyte-chemotactic protein, MCP-1; myeloperoxidase, MPO; serum amyloid A, SAA; adiponectin; leptin). Plaques in the aortic sinus were analysed for area, and content of collagen, lipid, macrophages and smooth muscle cells.RESULTS: High fat feeding resulted in marked increases in body mass and plasma lipid levels. Dietary TEMPOL decreased both parameters. In the high-fat-fed mice significant elevations in plasma lipid levels and the inflammatory markers IL-6, MCP-1, MPO, SAA were detected, along with an increase in leptin and a decrease in adiponectin. TEMPOL supplementation reversed these effects. When compared to HFD-fed mice, TEMPOL supplementation increased plaque collagen content, decreased lipid content and increased macrophage numbers.CONCLUSIONS: These data indicate that in a well-established model of obesity-associated hyperlipidaemia and atherosclerosis, TEMPOL had a significant impact on body mass, atherosclerosis, hyperlipidaemia and inflammation. TEMPOL may therefore be of value in suppressing obesity, metabolic disorders and increasing atherosclerotic plaque stability.

AB - OBJECTIVE: The nitroxide compound TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl radical) has been shown to prevent obesity-induced changes in adipokines in cell and animal systems. In this study we investigated whether supplementation with TEMPOL inhibits inflammation and atherosclerosis in apoE(-/-) mice fed a high fat diet (HFD).METHODS: ApoE(-/-) mice were fed for 12 weeks on standard chow diet or a high-fat diet. Half the mice were supplemented with 10 mg/g TEMPOL in their food. Plasma samples were analysed for triglycerides, cholesterol, low- and high-density lipoprotein cholesterol, inflammatory cytokines and markers (interleukin-6, IL-6; monocyte-chemotactic protein, MCP-1; myeloperoxidase, MPO; serum amyloid A, SAA; adiponectin; leptin). Plaques in the aortic sinus were analysed for area, and content of collagen, lipid, macrophages and smooth muscle cells.RESULTS: High fat feeding resulted in marked increases in body mass and plasma lipid levels. Dietary TEMPOL decreased both parameters. In the high-fat-fed mice significant elevations in plasma lipid levels and the inflammatory markers IL-6, MCP-1, MPO, SAA were detected, along with an increase in leptin and a decrease in adiponectin. TEMPOL supplementation reversed these effects. When compared to HFD-fed mice, TEMPOL supplementation increased plaque collagen content, decreased lipid content and increased macrophage numbers.CONCLUSIONS: These data indicate that in a well-established model of obesity-associated hyperlipidaemia and atherosclerosis, TEMPOL had a significant impact on body mass, atherosclerosis, hyperlipidaemia and inflammation. TEMPOL may therefore be of value in suppressing obesity, metabolic disorders and increasing atherosclerotic plaque stability.

U2 - 10.1016/j.atherosclerosis.2015.03.012

DO - 10.1016/j.atherosclerosis.2015.03.012

M3 - Journal article

C2 - 25818249

VL - 240

SP - 234

EP - 241

JO - Atherosclerosis

JF - Atherosclerosis

SN - 0021-9150

IS - 1

ER -

ID: 138272008