Thomas Damgaard Sandahl

Tumor necrosis factor-alpha acutely up-regulates urea synthesis in vivo in rats - a hepatic component of inflammatory catabolism?

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Tumor necrosis factor-alpha acutely up-regulates urea synthesis in vivo in rats - a hepatic component of inflammatory catabolism? / Thomsen, Karen Louise; Nielsen, Susanne Schouw; Aagaard, Niels Kristian; Sandahl, Thomas Damgaard; Grønbæk, Henning; Frystyk, Jan; Flyvbjerg, Allan; Vilstrup, Hendrik.

In: Scandinavian Journal of Clinical and Laboratory Investigation. Supplement, Vol. 70, No. 3, 2010, p. 151-7.

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@article{4fce8d60170b11dfb95d000ea68e967b,
title = "Tumor necrosis factor-alpha acutely up-regulates urea synthesis in vivo in rats - a hepatic component of inflammatory catabolism?",
abstract = "Abstract Background. Catabolism is a serious problem in patients with active inflammation. The tissue nitrogen (N) depletion is related to increased hepatic capacity for elimination of N via conversion of amino-N into urea-N. This is caused by the inflammatory process, but the mediators responsible are unknown. Tumor necrosis factor-alpha (TNF-alpha) plays a key role in inflammation, and we hypothesized that TNF-alpha up-regulates urea synthesis. Methods. We examined the in vivo capacity of urea-N synthesis (CUNS) and mRNA levels of urea cycle enzyme genes 3 h after TNF-alpha injection in rats. Circulating concentrations of glucagon, corticosterone, insulin, glucose, cytokines and acute phase proteins and their liver tissue gene expressions were measured. Results. TNF-alpha increased CUNS by 40% (p=0.03) despite decreased urea-cycle enzyme gene expression. TNF-alpha increased interleukin 6 (IL-6) (p < 0.001); circulating acute phase proteins were unchanged. Conclusion. TNF-alpha in rats caused an acute up-regulation of the in vivo capacity of urea synthesis which may promote loss of nitrogen from the body and catabolism. The results indicate that TNF-alpha has a post-transcriptional effect on regulation of urea synthesis that is independent of the acute phase protein synthesis. Effects of IL-6 may be involved.",
author = "Thomsen, {Karen Louise} and Nielsen, {Susanne Schouw} and Aagaard, {Niels Kristian} and Sandahl, {Thomas Damgaard} and Henning Gr{\o}nb{\ae}k and Jan Frystyk and Allan Flyvbjerg and Hendrik Vilstrup",
year = "2010",
doi = "10.3109/00365511003599537",
language = "English",
volume = "70",
pages = "151--7",
journal = "Scandinavian Journal of Clinical and Laboratory Investigation. Supplement",
issn = "0085-591X",
publisher = "Taylor & Francis A B",
number = "3",

}

RIS

TY - JOUR

T1 - Tumor necrosis factor-alpha acutely up-regulates urea synthesis in vivo in rats - a hepatic component of inflammatory catabolism?

AU - Thomsen, Karen Louise

AU - Nielsen, Susanne Schouw

AU - Aagaard, Niels Kristian

AU - Sandahl, Thomas Damgaard

AU - Grønbæk, Henning

AU - Frystyk, Jan

AU - Flyvbjerg, Allan

AU - Vilstrup, Hendrik

PY - 2010

Y1 - 2010

N2 - Abstract Background. Catabolism is a serious problem in patients with active inflammation. The tissue nitrogen (N) depletion is related to increased hepatic capacity for elimination of N via conversion of amino-N into urea-N. This is caused by the inflammatory process, but the mediators responsible are unknown. Tumor necrosis factor-alpha (TNF-alpha) plays a key role in inflammation, and we hypothesized that TNF-alpha up-regulates urea synthesis. Methods. We examined the in vivo capacity of urea-N synthesis (CUNS) and mRNA levels of urea cycle enzyme genes 3 h after TNF-alpha injection in rats. Circulating concentrations of glucagon, corticosterone, insulin, glucose, cytokines and acute phase proteins and their liver tissue gene expressions were measured. Results. TNF-alpha increased CUNS by 40% (p=0.03) despite decreased urea-cycle enzyme gene expression. TNF-alpha increased interleukin 6 (IL-6) (p < 0.001); circulating acute phase proteins were unchanged. Conclusion. TNF-alpha in rats caused an acute up-regulation of the in vivo capacity of urea synthesis which may promote loss of nitrogen from the body and catabolism. The results indicate that TNF-alpha has a post-transcriptional effect on regulation of urea synthesis that is independent of the acute phase protein synthesis. Effects of IL-6 may be involved.

AB - Abstract Background. Catabolism is a serious problem in patients with active inflammation. The tissue nitrogen (N) depletion is related to increased hepatic capacity for elimination of N via conversion of amino-N into urea-N. This is caused by the inflammatory process, but the mediators responsible are unknown. Tumor necrosis factor-alpha (TNF-alpha) plays a key role in inflammation, and we hypothesized that TNF-alpha up-regulates urea synthesis. Methods. We examined the in vivo capacity of urea-N synthesis (CUNS) and mRNA levels of urea cycle enzyme genes 3 h after TNF-alpha injection in rats. Circulating concentrations of glucagon, corticosterone, insulin, glucose, cytokines and acute phase proteins and their liver tissue gene expressions were measured. Results. TNF-alpha increased CUNS by 40% (p=0.03) despite decreased urea-cycle enzyme gene expression. TNF-alpha increased interleukin 6 (IL-6) (p < 0.001); circulating acute phase proteins were unchanged. Conclusion. TNF-alpha in rats caused an acute up-regulation of the in vivo capacity of urea synthesis which may promote loss of nitrogen from the body and catabolism. The results indicate that TNF-alpha has a post-transcriptional effect on regulation of urea synthesis that is independent of the acute phase protein synthesis. Effects of IL-6 may be involved.

U2 - 10.3109/00365511003599537

DO - 10.3109/00365511003599537

M3 - Journal article

C2 - 20141500

VL - 70

SP - 151

EP - 157

JO - Scandinavian Journal of Clinical and Laboratory Investigation. Supplement

JF - Scandinavian Journal of Clinical and Laboratory Investigation. Supplement

SN - 0085-591X

IS - 3

ER -