Effect of protein deficiency on endogenous pyrogen-mediated acute phase protein responses

1983 ◽  
Vol 61 (4) ◽  
pp. 376-380 ◽  
Author(s):  
R. Bell ◽  
L. Hoffman-Goetz

Endogenous pyrogen (EP) is known to trigger a rise in the plasma concentrations of various acute phase reactant proteins. This study describes the effects of chronic protein deficiency in rabbits on EP-mediated changes in the plasma concentrations of fibrinogen, albumin, and α2-macroglobulm. Injection (i.v.) of EP from healthy donors into protein-deprived rabbits produced a smaller rise in plasma fibrinogen and α2-maeroglobulin, and a smaller fall in plasma albumin than injection of EP into controls. Injection of EP, obtained from malnourished donors, into healthy rabbits also resulted in an attenuation of the acute phase protein response. These data are consistent with the hypothesis that EP activity is influenced by the nutritional status of both the donor and recipient of EP.

1996 ◽  
Vol 76 (1) ◽  
pp. 123-132 ◽  
Author(s):  
G. Jennings ◽  
M. Elia

The present study investigated the effect of the acute-phase ‘injury’ response, induced by subcutaneous injection of turpentine, on the hydration and protein content of organs and tissues of normally nourished rats receiving a diet containing 200g protein/kg, and of protein-malnourished rats receiving a diet containing 30 g protein/kg. The measurements were carried out 48 h after turpentine injection, and were compared with both saline-injected animals, and pair-fed control animals. Circulating α2-macroglobulin was also measured as an index of the acute-phase-protein response. In normally nourished rats turpentine injection caused a significant increase in the mean masses of the liver, kidney and lung (7–35% compared with saline-injected animals, and 20–44% compared with pair-fed controls), and a small reduction in the mass of extra-abdominal and extrathoracic tissues (‘carcass’). In general the protein content of tissues changed in a similar way (for liver, kidney and lung a 16–33% increase compared with saline-injected animals, and 32–49% compared with pair-fed controls). Protein deficiency produced a significant attenuation in the response to turpentine. The change in the mass and protein content of several tissues was reduced (for lung, liver and kidney, the increase in protein content was only 5–15%), and the effects on anorexia (1 v. 41% reduction infood intake) and the α2,-macroglobulin response (1·28 v. 4·28 g/l; P< 0·001) were also reduced. It is concluded that the injury response spares most central thoracic and abdominal organs, but this effect as well as the anorexia and acute-phase-protein response to injury are attenuated by protein deficiency.


1998 ◽  
Vol 275 (1) ◽  
pp. E112-E117 ◽  
Author(s):  
John F. Morlese ◽  
Terrence Forrester ◽  
Farook Jahoor

It is not known whether malnourished infants can mount a comprehensive acute-phase protein (APP) response and, if so, whether this is achieved by increasing APP synthesis rates. To address these issues, we measured 1) the plasma concentrations of five APPs (C-reactive protein, α1-acid glycoprotein, α1-antitrypsin, haptoglobin, and fibrinogen) and 2) the synthesis rates of three APPs (α1-antitrypsin, haptoglobin, and fibrinogen) using a constant intragastric infusion of [2H3]leucine in nine infected marasmic children at ∼2 days postadmission ( study 1), ∼9 days postadmission when infections had cleared ( study 2), and ∼59 days postadmission at recovery ( study 3). Except for fibrinogen, the plasma concentrations of all APPs were higher in study 1 than in studies 2 and 3. Although the rate of synthesis of haptoglobin was significantly greater in study 1 than study 2, the rates of fibrinogen and α1-antitrypsin synthesis were similar in all three studies. These results show that 1) severely malnourished children can mount an APP response to infection which does not include fibrinogen and 2) the APP response is accomplished through different mechanisms.


PLoS ONE ◽  
2020 ◽  
Vol 15 (3) ◽  
pp. e0230949
Author(s):  
Arash Janmohammadi ◽  
Nariman Sheikhi ◽  
Hadi Haghbin Nazarpak ◽  
Gholamreza Nikbakht Brujeni

1998 ◽  
Vol 274 (6) ◽  
pp. R1518-R1525 ◽  
Author(s):  
Atsushi Kaibara ◽  
Armin Moshyedi ◽  
Troy Auffenberg ◽  
Amer Abouhamze ◽  
Edward M. Copeland ◽  
...  

The ob gene product leptin is known to produce anorexia and loss of body fat when chronically administered to both lean and genetically obese mice. The current study was undertaken to examine whether administration of recombinant leptin in quantities sufficient to produce decreases in food intake and body weight and alterations in body composition would elicit either an hepatic acute phase protein response or preferential loss of carcass lean tissue. Mice were administered increasing quantities of recombinant human leptin or human tumor necrosis factor-α as a positive control. Although leptin (at 10 mg/kg body wt) produced significant anorexia and weight loss (both P < 0.05), human leptin administration did not appear to induce an hepatic acute phase protein response in either lean or genetically obese mice, as determined by protein synthetic rates in the liver or changes in the plasma concentration of the murine acute phase protein reactants, amyloid A, amyloid P, or seromucoid (α1-acid glycoprotein). In addition, human leptin administration did not induce a loss of fat-free dry mass (protein) in lean or obese animals. The findings suggest that at doses adequate to alter food intake and body weight leptin is not a significant inducer of the hepatic acute phase response nor does leptin promote the preferential loss of somatic protein characteristic of a chronic inflammatory process.


Sign in / Sign up

Export Citation Format

Share Document