Chronic TNF Infusion Causes Anorexia But Not Accelerated Nitrogen Loss

Michie, Hamish R.; Sherman, Matthew L.; Spriggs, David R.; Rounds, Jan D.; Christie, Michael; Wilmore, Douglas W.

doi:10.1097/00000658-198901000-00002

Cited by 87 publications

(28 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: 70%

“…Few studies of comparable design have been conducted in humans. In one, an almost complete cessation of food intake was reported following the intravenous infusion of TNFa in adult elective surgical patients (Michie et al, 1989). The association between serum IL-1b and reduced energy intake also was described in animal studies.…”

Section: Discussionmentioning

confidence: 95%

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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: 70%

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

et al. 2007

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“…First, both leptin and TNFa are produced by adipose tissue proportionally to the amount of fat stores 11Y12Y27À29 and are capable of affecting feeding behaviour and energy Leptin and TNFa system in the obese F Corica et al expenditure. 6,30,31 Second, leptin and TNFa production seem to be enhanced through the same pathways 18,32 and their mRNA expression increases during weight gain and falls during weight loss. 12,28 Third and ®nally, lower plasma leptin levels have been found in TNFa-de®cient mice with respect to wild-type animals, 19 and TNFa administration has been shown to be able to increase circulating leptin concentrations in patients with solid tumors.…”

Section: Discussionmentioning

confidence: 99%

Relationship between plasma leptin levels and the tumor necrosis factor-α system in obese subjects

et al. 1999

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OBJECTIVE: To evaluate the relationship between plasma leptin and the tumor necrosis factor-a (TNFa), TNF receptor p60 (TNF-R1) and TNF receptor p80 (TNF-R2) concentrations in obese subjects. DESIGN: Case-control study. SETTING: Outpatient's Service for Prevention and Treatment of Obesity at the University Hospital. MEASUREMENTS: Body mass index (BMI), waist circumference, hip circumference, waist-to-hip ratio (WHR), fasting plasma glucose, fasting plasma insulin, homeostasis model assessment of insulin resistance (HOMA IR), plasma leptin, TNFa a, TNF-R1 and TNF-R2 concentrations were evaluated in obese subjects (n 42) and in age-and gendermatched, lean healthy controls (n 16). RESULTS: In obese subjects, fasting plasma glucose and insulin, HOMA IR, plasma leptin, TNFa a, TNF-R1 and TNF-R2 concentrations were signi®cantly higher than in controls. Furthermore, females showed higher leptin, TNF-R1 and TNF-R2 plasma concentrations compared to males, in both control and obese subjects. In control subjects, plasma leptin concentrations showed a direct correlation with BMI (r 0.74, P`0.001), hip circumference (r 0.94, P`0.001), TNF-R1 (r 0.79, P`0.001) and TNF-R2 (r 0.64, P`0.01), and a negative correlation with WHR (r À À0.58, P`0.05). In obese subjects, we found a direct correlation between plasma leptin concentrations and BMI (r 0.67, P`0.001), hip circumference (r 0.66, P`0.001), fasting glucose (r 0.37, P`0.05), fasting insulin (r 0.31, P`0.05), HOMA IR (r 0.38, P`0.05), TNF-R1 (r 0.71, P`0.001) and TNR-R2 (r 0.66, P`0.001), while a negative correlation was found between circulating leptin and WHR (r À À0.44, P`0.01). In multivariate analysis, plasma leptin concentrations were signi®cantly associated with BMI (P 0.015) and gender (P 0.047) in the control group, while in obese subjects, plasma leptin showed a signi®cant association with BMI (P 0.019) and TNF-R1 (P 0.012). CONCLUSIONS: Our results are consistent with the hypothesis that the TNFa a system could be involved in the regulation of plasma leptin concentrations in obese subjects.

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“…Whether TNF-␣ alone is sufficient to cause muscle atrophy in vivo, however, is controversial. Accelerated muscle protein degradation or decreased protein content has been reported after TNF-␣ administration in some studies but not in others (10,15,16,29,33,36).…”

mentioning

confidence: 95%

Tumor necrosis factor-α promotes the accumulation of neutrophils and macrophages in skeletal muscle

Peterson¹,

Feeback²,

Baas³

et al. 2006

Journal of Applied Physiology

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Chronic TNF Infusion Causes Anorexia But Not Accelerated Nitrogen Loss

Cited by 87 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

Relationship between plasma leptin levels and the tumor necrosis factor-α system in obese subjects

Tumor necrosis factor-α promotes the accumulation of neutrophils and macrophages in skeletal muscle

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