Publication

High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice

van der Heijden, R. A., Sheedfar, F., Morrison, M. C., Hommelberg, P. P. H., Kor, D., Kloosterhuis, N. J., Gruben, N., Youssef, S. A., de Bruin, A., Hofker, M. H., Kleemann, R., Koonen, D. P. Y. & Heeringa, P., Apr-2015, In : Aging. 7, 4, p. 256-268 13 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

van der Heijden, R. A., Sheedfar, F., Morrison, M. C., Hommelberg, P. P. H., Kor, D., Kloosterhuis, N. J., ... Heeringa, P. (2015). High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice. Aging, 7(4), 256-268. https://doi.org/10.18632/aging.100738

Author

van der Heijden, Roel A. ; Sheedfar, Fareeba ; Morrison, Martine C. ; Hommelberg, Pascal P. H. ; Kor, Danny ; Kloosterhuis, Niels J. ; Gruben, Nanda ; Youssef, Sameh A. ; de Bruin, Alain ; Hofker, Marten H. ; Kleemann, Robert ; Koonen, Debby P. Y. ; Heeringa, Peter. / High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice. In: Aging. 2015 ; Vol. 7, No. 4. pp. 256-268.

Harvard

van der Heijden, RA, Sheedfar, F, Morrison, MC, Hommelberg, PPH, Kor, D, Kloosterhuis, NJ, Gruben, N, Youssef, SA, de Bruin, A, Hofker, MH, Kleemann, R, Koonen, DPY & Heeringa, P 2015, 'High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice', Aging, vol. 7, no. 4, pp. 256-268. https://doi.org/10.18632/aging.100738

Standard

High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice. / van der Heijden, Roel A.; Sheedfar, Fareeba; Morrison, Martine C.; Hommelberg, Pascal P. H.; Kor, Danny; Kloosterhuis, Niels J.; Gruben, Nanda; Youssef, Sameh A.; de Bruin, Alain; Hofker, Marten H.; Kleemann, Robert; Koonen, Debby P. Y.; Heeringa, Peter.

In: Aging, Vol. 7, No. 4, 04.2015, p. 256-268.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

van der Heijden RA, Sheedfar F, Morrison MC, Hommelberg PPH, Kor D, Kloosterhuis NJ et al. High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice. Aging. 2015 Apr;7(4):256-268. https://doi.org/10.18632/aging.100738


BibTeX

@article{6ad7da19733d4114a3c3b66b8207209d,
title = "High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice",
abstract = "Metabolic inflammation in adipose tissue and the liver is frequently observed as a result of diet-induced obesity in human and rodent studies. Although the adipose tissue and the liver are both prone to become chronically inflamed with prolonged obesity, their individual contribution to the development of metabolic inflammation remains speculative. Thus, we aimed to elucidate the sequence of inflammatory events in adipose and hepatic tissues to determine their contribution to the development of metabolic inflammation and insulin resistance (IR) in diet-induced obesity. To confirm our hypothesis that adipose tissue (AT) inflammation is initiated prior to hepatic inflammation, C57BL/6J male mice were fed a low-fat diet (LFD; 10{\%} kcal fat) or high-fat diet (HFD; 45{\%} kcal fat) for either 24, 40 or 52 weeks. Lipid accumulation and inflammation was measured in AT and liver. Glucose tolerance was assessed and plasma levels of glucose, insulin, leptin and adiponectin were measured at various time points throughout the study. With HFD, C57BL/6j mice developed a progressive obese phenotype, accompanied by IR at 24 and 40 weeks of HFD, but IR was attenuated after 52 weeks of HFD. AT inflammation was present after 24 weeks of HFD, as indicated by the increased presence of crown-like structures and up-regulation of pro-inflammatory genesTnf, Il1β, Mcp1 and F4/80. As hepatic inflammation was not detected until 40 weeks of HFD, we show that AT inflammation is established prior to the development of hepatic inflammation. Thus, AT inflammation is likely to have a greater contribution to the development of IR compared to hepatic inflammation.",
keywords = "obesity, metabolic syndrome, insulin resistance, inflammation, adipose tissue, NASH, liver, INSULIN-RESISTANCE, NONALCOHOLIC STEATOHEPATITIS, METABOLIC SYNDROME, GLUCOSE-TOLERANCE, HEPATIC STEATOSIS, DISEASE, AGE, EXPRESSION, RAPAMYCIN, STRESS",
author = "{van der Heijden}, {Roel A.} and Fareeba Sheedfar and Morrison, {Martine C.} and Hommelberg, {Pascal P. H.} and Danny Kor and Kloosterhuis, {Niels J.} and Nanda Gruben and Youssef, {Sameh A.} and {de Bruin}, Alain and Hofker, {Marten H.} and Robert Kleemann and Koonen, {Debby P. Y.} and Peter Heeringa",
year = "2015",
month = "4",
doi = "10.18632/aging.100738",
language = "English",
volume = "7",
pages = "256--268",
journal = "Aging",
issn = "1945-4589",
publisher = "Impact Journals LLC",
number = "4",

}

RIS

TY - JOUR

T1 - High-fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice

AU - van der Heijden, Roel A.

AU - Sheedfar, Fareeba

AU - Morrison, Martine C.

AU - Hommelberg, Pascal P. H.

AU - Kor, Danny

AU - Kloosterhuis, Niels J.

AU - Gruben, Nanda

AU - Youssef, Sameh A.

AU - de Bruin, Alain

AU - Hofker, Marten H.

AU - Kleemann, Robert

AU - Koonen, Debby P. Y.

AU - Heeringa, Peter

PY - 2015/4

Y1 - 2015/4

N2 - Metabolic inflammation in adipose tissue and the liver is frequently observed as a result of diet-induced obesity in human and rodent studies. Although the adipose tissue and the liver are both prone to become chronically inflamed with prolonged obesity, their individual contribution to the development of metabolic inflammation remains speculative. Thus, we aimed to elucidate the sequence of inflammatory events in adipose and hepatic tissues to determine their contribution to the development of metabolic inflammation and insulin resistance (IR) in diet-induced obesity. To confirm our hypothesis that adipose tissue (AT) inflammation is initiated prior to hepatic inflammation, C57BL/6J male mice were fed a low-fat diet (LFD; 10% kcal fat) or high-fat diet (HFD; 45% kcal fat) for either 24, 40 or 52 weeks. Lipid accumulation and inflammation was measured in AT and liver. Glucose tolerance was assessed and plasma levels of glucose, insulin, leptin and adiponectin were measured at various time points throughout the study. With HFD, C57BL/6j mice developed a progressive obese phenotype, accompanied by IR at 24 and 40 weeks of HFD, but IR was attenuated after 52 weeks of HFD. AT inflammation was present after 24 weeks of HFD, as indicated by the increased presence of crown-like structures and up-regulation of pro-inflammatory genesTnf, Il1β, Mcp1 and F4/80. As hepatic inflammation was not detected until 40 weeks of HFD, we show that AT inflammation is established prior to the development of hepatic inflammation. Thus, AT inflammation is likely to have a greater contribution to the development of IR compared to hepatic inflammation.

AB - Metabolic inflammation in adipose tissue and the liver is frequently observed as a result of diet-induced obesity in human and rodent studies. Although the adipose tissue and the liver are both prone to become chronically inflamed with prolonged obesity, their individual contribution to the development of metabolic inflammation remains speculative. Thus, we aimed to elucidate the sequence of inflammatory events in adipose and hepatic tissues to determine their contribution to the development of metabolic inflammation and insulin resistance (IR) in diet-induced obesity. To confirm our hypothesis that adipose tissue (AT) inflammation is initiated prior to hepatic inflammation, C57BL/6J male mice were fed a low-fat diet (LFD; 10% kcal fat) or high-fat diet (HFD; 45% kcal fat) for either 24, 40 or 52 weeks. Lipid accumulation and inflammation was measured in AT and liver. Glucose tolerance was assessed and plasma levels of glucose, insulin, leptin and adiponectin were measured at various time points throughout the study. With HFD, C57BL/6j mice developed a progressive obese phenotype, accompanied by IR at 24 and 40 weeks of HFD, but IR was attenuated after 52 weeks of HFD. AT inflammation was present after 24 weeks of HFD, as indicated by the increased presence of crown-like structures and up-regulation of pro-inflammatory genesTnf, Il1β, Mcp1 and F4/80. As hepatic inflammation was not detected until 40 weeks of HFD, we show that AT inflammation is established prior to the development of hepatic inflammation. Thus, AT inflammation is likely to have a greater contribution to the development of IR compared to hepatic inflammation.

KW - obesity

KW - metabolic syndrome

KW - insulin resistance

KW - inflammation

KW - adipose tissue

KW - NASH

KW - liver

KW - INSULIN-RESISTANCE

KW - NONALCOHOLIC STEATOHEPATITIS

KW - METABOLIC SYNDROME

KW - GLUCOSE-TOLERANCE

KW - HEPATIC STEATOSIS

KW - DISEASE

KW - AGE

KW - EXPRESSION

KW - RAPAMYCIN

KW - STRESS

U2 - 10.18632/aging.100738

DO - 10.18632/aging.100738

M3 - Article

VL - 7

SP - 256

EP - 268

JO - Aging

JF - Aging

SN - 1945-4589

IS - 4

ER -

ID: 19753623