Changes in thermogenesis and brown fat activity in response to tumour necrosis factor in the rat

1987 ◽  
Vol 7 (10) ◽  
pp. 791-799 ◽  
Author(s):  
R. C. Coombes ◽  
N. J. Rothwell ◽  
P. Shah ◽  
M. J. Stock
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Adrenergic Blockade ◽  
Adult Rats ◽  
Bat Activity ◽  
Brown Adipose ◽  
Human Tumour Necrosis Factor ◽  
Necrosis Factor

A single intravenous injection of recombinant human tumour necrosis factor (TNF) resulted in significant, but transient (24–48 hr) reductions in food intake and body weight, and increases in rectal temperature, resting oxygen consumption (VO2) and brown adipose tissue (BAT) thermogenic activity (mitochondrial GDP-binding). The increased VO2 was inhibited by β-adrenergic blockade (propranolol), and activation of BAT was prevented by denervation of the tissue. In adult (4-month old) animals, TNF induced greater reductions in food intake and body weight, caused general malaise and some fatalities, but did not significantly alter VO2 or BAT activity. However, the reduction in VO2 following β-adrenergic blockade was greater in TNF-treated rats and BAT activity was enhanced when compared to pair-fed controls. Injection of adult rats with gamma-interferon induced small changes in body weight and temperature which were slightly potentiated when injected with a low dose of TNF. The results indicate that TNF stimulates sympathetic outflow to BAT. This effect may be partly responsible for the increases in body temperature and metabolic rate associated with TNF treatment and with cancer cachexia.

Human tumour necrosis factor: precursor structure, expression and homology to lymphotoxin

Nature ◽  
1984 ◽  
Vol 312 (5996) ◽  
pp. 724-729 ◽  
Author(s):  
Diane Pennica ◽  
Glenn E. Nedwin ◽  
Joel S. Hayflick ◽  
Peter H. Seeburg ◽  
Rik Derynck ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Human Tumour ◽  
Precursor Structure ◽  
Human Tumour Necrosis Factor ◽  
Necrosis Factor

Expression and rescuing of a cloned human tumour necrosis factor gene using an EBV-based shuttle cosmid vector.

1987 ◽  
Vol 6 (2) ◽  
pp. 355-361 ◽  
Author(s):  
D. Kioussis ◽  
F. Wilson ◽  
C. Daniels ◽  
C. Leveton ◽  
J. Taverne ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Human Tumour ◽  
Factor Gene ◽  
Human Tumour Necrosis Factor ◽  
Cosmid Vector ◽  
Necrosis Factor

Cloning and expression in Escherichia coli of the gene for human tumour necrosis factor

Nature ◽  
1985 ◽  
Vol 313 (6005) ◽  
pp. 803-806 ◽  
Author(s):  
Takashi Shirai ◽  
Hiroshi Yamaguchi ◽  
Hirataka Ito ◽  
Chas. W. Todd ◽  
R. Bruce Wallace
Keyword(s):  
Escherichia Coli ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Cloning And Expression ◽  
Human Tumour ◽  
Expression In Escherichia Coli ◽  
Human Tumour Necrosis Factor ◽  
Necrosis Factor

Role of serum cytokines tumour necrosis factor-αand interleukin-6 in the association between body weight and periodontal infection

2009 ◽  
Vol 36 (2) ◽  
pp. 100-105 ◽  
Author(s):  
Tuomas Saxlin ◽  
Liisa Suominen-Taipale ◽  
Jaana Leiviskä ◽  
Antti Jula ◽  
Matti Knuuttila ◽  
...  
Keyword(s):  
Body Weight ◽  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Tumour Necrosis ◽  
Serum Cytokines ◽  
Periodontal Infection ◽  
Necrosis Factor

Transgenic mice expressing human tumour necrosis factor: a predictive genetic model of arthritis.

1991 ◽  
Vol 10 (13) ◽  
pp. 4025-4031 ◽  
Author(s):  
J. Keffer ◽  
L. Probert ◽  
H. Cazlaris ◽  
S. Georgopoulos ◽  
E. Kaslaris ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Genetic Model ◽  
Human Tumour ◽  
Human Tumour Necrosis Factor ◽  
Necrosis Factor

Model for Whole Body Production of Tumour Necrosis Factor-α in Experimental Endotoxaemia in Healthy Subjects

1994 ◽  
Vol 87 (4) ◽  
pp. 459-465 ◽  
Author(s):  
R. Koopmans ◽  
F. J. Hoek ◽  
S. J. H. van Deventer ◽  
T. van der Poll
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Whole Body ◽  
Serum Concentrations ◽  
Tumour Necrosis Factor Α ◽  
Human Tumour ◽  
Human Tumour Necrosis Factor ◽  
Body Production ◽  
Factor Α ◽  
Necrosis Factor

1. Tumour necrosis factor-α is considered an important mediator in the pathophysiology of several diseases. Although much information is available about the serum concentrations of this cytokine in these illnesses, little is known about the production of tumour necrosis factor-α in disease in vivo. 2. In the present study we aimed to estimate the extent and the kinetics of whole body tumour necrosis factor-α synthesis in experimental endotoxaemia in six healthy humans. For this purpose we first examined the pharmacokinetic behaviour of an intravenously injected bolus of recombinant human tumour necrosis factor-α (50 μg/m2) in another group of six normal subjects. We then calculated the total amount of tumour necrosis factor-α produced after intravenous injection of endotoxin (2 ng/kg) as the product of the systemic clearance of recombinant human tumour necrosis factor-α (9.5 ± 5.0 ml min−1 kg−1) and the area under the tumour necrosis factor-α concentration-time curves in the endotoxaemic subjects. 3. Recombinant human tumour necrosis factor-α showed evident two-compartment kinetics with an initial rapid disappearance (t1/2 5.1 ± 2.2 min) and a terminal slower elimination (t1/2 49 ± 5 min). Tumour necrosis factor-α synthesis after endotoxin varied markedly between individuals, ranging from 11.8 to 114.1 μg (52.7 ± 34.7 μg). The changes in time of the serum concentrations of tumour necrosis factor-α after administration of endotoxin could be accurately described with an adapted two-compartment open model that incorporated both rapid tumour necrosis factor-α production (74% of the total amount) and slow tumour necrosis factor-α production (26%). 4. Our results suggest that, in endotoxaemia, circulating tumour necrosis factor-α originates from two different sources, one in rapid and one in slow equilibrium with the circulation. We propose that the pharmacokinetic characteristics of intravenous recombinant human tumour necrosis factor-α may be used to estimate the production of rumour necrosis factor-α in clinical disease.

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