Recombinant human tumor necrosis factor induces acute reductions in food intake and body weight in mice.

Socher, Susan H.; Friedman, Arthur; Martinez, Douglas

doi:10.1084/jem.167.6.1957

Cited by 109 publications

(57 citation statements)

References 14 publications

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“…Similar studies of TNFa or IL-1b, however, have not been reported in infants, either in humans or in animal models. Nonetheless, increases in cytokines and reductions in energy intakes observed in these investigations are consistent with the limited available animal and human studies and other reports associating proinflammatory cytokines to anorectic response to infections (McCarthy et al, 1985;Socher et al, 1988;Michie et al, 1989).…”

Section: Discussionsupporting

confidence: 91%

“…These and related observations in human and animal studies (McCarthy et al, 1985;Socher et al, 1988;Michie et al, 1989) also suggest that DHA and EPA supplementation may attenuate anorectic responses to infectious illness.…”

Section: Introductionmentioning

confidence: 68%

“…Inhibition of food intake that persisted for 2 days was reported in mice given exogenous TNFa by either bolus injection or continuous infusion (Socher et al, 1988). Few studies of comparable design have been conducted in humans.…”

Section: Discussionmentioning

confidence: 99%

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Breastfeeding's protection against illness-induced anorexia is mediated partially by docosahexaenoic acid

et al. 2007

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Objective: To test whether breastfeeding's protection against anorectic responses to infection is mediated by nÀ3 fatty acids' attenuation of interleukin (IL)-1b and tumor necrosis factor (TNF)a. Design: Experimental and observational studies. Setting: A hospital-based study was conducted. Subjects: Five groups of infants were followed; three in the experimental and two in the observational study. Methods: Breast-fed-(BF-1), DHA-supplemented formula-(SFF-1), and non-DHA-supplemented formula-fed (FF-1) infants were studied before and after immunization against diphtheria, tetanus, pertussis and haemophilus influenzae type b. Pre-and postimmunization energy intakes (EI) and serum IL-1b and TNFa were measured. The two other groups, breast-fed (BF-2) and formula-fed (FF-2) infants with pneumonia were followed throughout hospitalization. EI, IL-1b and TNFa were measured at admission and discharge. Baseline erythrocyte fatty acid contents were determined. Results: Both cytokines increased following immunization in all feeding groups. Post-immunization reductions in EI of SFF-1 infants (À11.875%, CI 95 ¼ À23.3, 1.4%, P ¼ 0.07) were intermediate to those observed in BF-1 (À5.274.2%, CI 95 ¼ À15.2, 5.9%, P ¼ 0.27) and FF-1 infants (À1874.4%, CI 95 ¼ À29%, À5.4%, P ¼ 0.02). In the observational study, TNFa (17.278.3 vs 3.473.0 ng/l, P ¼ 0.001) and decreases in EI (À31743 vs À15731%, CI 95 ¼ À34%, 0.001%, P ¼ 0.056) were greater in FF-2 than in BF-2 infants at admission. Breastfeeding duration was associated positively with docosahexaenoic acid (DHA) erythrocyte contents, and negatively with admission TNFa. Decreases in EIs were associated with IL-1b and TNFa concentrations. Conclusion: Reductions in EI following immunologic or infectious stimuli were associated with increases in IL-1b and TNFa. Those reductions were attenuated by breastfeeding, and mediated in part by tissue DHA. Sponsorship: This research was supported by grants from the Nestlé Foundation and the CONACYT Mexico. Nutricia Kasdorf (Buenos Aires, Argentina) provided supplemented and unsupplemented formulas.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 68%

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Breastfeeding's protection against illness-induced anorexia is mediated partially by docosahexaenoic acid

et al. 2007

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“…There is some evidence from in vivo studies that the potent cytokine TNF 1 (2) is able to induce tolerance-like conditions. For example, pretreatment with TNF in several animal species selectively affects certain TNF effects such as fever, anorexia, and lethality (3)(4)(5) and partially affects gastrointestinal toxicity (6). Cyclooxygenase inhibitors prevent the induction of tolerance to the toxic effect of TNF (7).…”

mentioning

confidence: 99%

Transcriptional Inhibition of Interleukin-8 Expression in Tumor Necrosis Factor-tolerant Cells

Weber

Sydlik

Quirling

et al. 2003

Journal of Biological Chemistry

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There is some evidence that the potent cytokine tumor necrosis factor (TNF) is able to induce tolerance after repeated stimulation of cells. To investigate the molecular mechanisms mediating this phenomenon, the expression of interleukin-8 (IL-8), which is regulated by transcription factors NF-B and C/EBP␤, was monitored under TNF tolerance conditions. Pretreatment of monocytic cells for 72 h with low TNF doses inhibited TNFinduced (restimulation with a high dose) IL-8 promoterdependent transcription as well as IL-8 production. Under these conditions neither activation of NF-B nor I B proteolysis was affected after TNF re-stimulation, albeit a slightly reduced I B-␣ level was found in the TNF pretreated but not re-stimulated sample. Remarkably, in tolerant cells an increased binding of C/EBP␤ to its IL-8 promoter-specific DNA motif as well as an elevated association of C/EBP␤ protein with p65-containing NF-B complexes was observed. Finally, overexpression of C/EBP␤, but not p65 or Oct-1, markedly prevented TNFinduced IL-8 promoter-dependent transcription. Taken together, these data indicate that the expression of IL-8 is inhibited at the transcriptional level in TNF-tolerant cells and C/EBP␤ is involved under these conditions in mediating the negative-regulatory effects, a mechanism that may play a role in inflammatory processes such as sepsis.

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“…69(9): 931-937, 2007 Anorexia and weight loss are frequently associated with acute or chronic infections [11,24]. Since several inflammatory cytokines, most notably TNFα and IL-1β, have been shown to induce anorexia and weight loss, it appears to be likely that these cytokines mediate metabolic changes of infection [9,18,23,26,27,35,37]. However, the mechanisms and mediators by which infection induces anorexia are still poorly understood.…”

mentioning

confidence: 99%

The Ay allele at the agouti Locus Enhances Sensitivity to Endotoxin-Induced Lethality in Mice

Suto

2007

The Journal of Veterinary Medical Science

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ABSTRACT. In the course of investigations on anorexia during infection, I found that B6-A y mice had significantly increased sensitivity to lipopolysaccharide (LPS)-induced lethality as compared with isogenic B6 mice. I also found that the sensitivity to the lethal effect of LPS dramatically increased in aged mice (age effect), both B6 and B6-A y . However, the A y effect of enhancing sensitivity to LPS-induced lethality was still significant, suggesting that the A y effect is independent of age. In the absence of tumor necrosis factor α (TNFα), the A y effect was still significant, suggesting that the A y effect is independent of TNFα toxicity. A dose of LPS of 100 µg per mouse caused 15% lethality in B6, 65% in B6-A y (significantly higher than B6), and 100 % in leptin-deficient B6-ob/ob (significantly higher than B6 and B6-A y ). The results support the hypothesis that endogenous leptin has a protective role against infection, and that a part of this leptin effect is mediated by α-melanocyte-stimulating hormone (αMSH). In contrast to the results of simple blockade at the melanocortin 4 receptor (MC4R), B6-A y suffered more severe LPS-induced anorexia than did B6; therefore, the pathway involving MC4R is not absolutely required for the LPS-induced anorexia, and the presence of pathways involving other melanocortin receptor types was suggested. Because αMSH is suggested to be an endogenous anti-inflammatory peptide, and because melanocortin 1 receptor (MC1R) is expressed in various cutaneous cell types, the A y effect might be caused via the pathway involving MC1R. Physiologic significance of αMSH-MC1R interaction in host defense against infection is discussed. KEY WORDS: anorexia, A y allele, lethality, lipopolysaccharide (LPS), melanocortin receptors.J. Vet. Med. Sci. 69(9): 931-937, 2007 Anorexia and weight loss are frequently associated with acute or chronic infections [11,24]. Since several inflammatory cytokines, most notably TNFα and IL-1β, have been shown to induce anorexia and weight loss, it appears to be likely that these cytokines mediate metabolic changes of infection [9,18,23,26,27,35,37]. However, the mechanisms and mediators by which infection induces anorexia are still poorly understood. For experimental induction of an inflammatory response, lipopolysaccharide (LPS, gramnegative bacterial endotoxin) has been extensively used. LPS administration causes anorexia [5,6,11,15,24,32]. Toxic effects exerted by LPS are largely mediated by the effects of cytokines including the above-mentioned ones; thus, LPS administration is used as a model of systemic infection [5,6,32].It is now widely recognized that the central regulator of food intake and body weight is leptin [38]. Leptin expression can be induced by the inflammatory cytokines and LPS administration; therefore, it was once postulated that leptin is a mediator of anorexia during infection [11,24]. However, subsequent studies revealed that functional leptin system was not essential in LPS-induced anorexia, because LPS caused anorexia in both l...

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Recombinant human tumor necrosis factor induces acute reductions in food intake and body weight in mice.

Cited by 109 publications

References 14 publications

Breastfeeding's protection against illness-induced anorexia is mediated partially by docosahexaenoic acid

Breastfeeding's protection against illness-induced anorexia is mediated partially by docosahexaenoic acid

Transcriptional Inhibition of Interleukin-8 Expression in Tumor Necrosis Factor-tolerant Cells

The Ay allele at the agouti Locus Enhances Sensitivity to Endotoxin-Induced Lethality in Mice

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