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Journal articles on the topic 'Tumor Necrosis Factor/metabolism'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Kaji, Keisuke, Rei Katogi, Yoshiaki Azuma, Asuka Naito, Jun-Ichiro Inoue та Akira Kudo. "Tumor Necrosis Factor α-Induced Osteoclastogenesis Requires Tumor Necrosis Factor Receptor-Associated Factor 6". Journal of Bone and Mineral Research 16, № 9 (2001): 1593–99. http://dx.doi.org/10.1359/jbmr.2001.16.9.1593.

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2

Balkwill, Fran. "Tumor necrosis factor or tumor promoting factor?" Cytokine & Growth Factor Reviews 13, no. 2 (2002): 135–41. http://dx.doi.org/10.1016/s1359-6101(01)00020-x.

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3

Wu, Shanshan, Kai Dong, Jiajia Wang, and Yaxin Bi. "Tumor necrosis factor alpha improves glucose homeostasis in diabetic mice independent with tumor necrosis factor receptor 1 and tumor necrosis factor receptor 2." Endocrine Journal 65, no. 6 (2018): 601–9. http://dx.doi.org/10.1507/endocrj.ej17-0539.

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4

Holeček, M. "Leucine metabolism in fasted and tumor necrosis factor-treated rats." Clinical Nutrition 15, no. 2 (1996): 91–93. http://dx.doi.org/10.1016/s0261-5614(96)80028-8.

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5

Battelino, Tadej, Masakatsu Goto, Ciril Krzisnik та W. Patrick Zeller. "Tumor necrosis factor-α alters glucose metabolism in suckling rats". Journal of Laboratory and Clinical Medicine 133, № 6 (1999): 583–89. http://dx.doi.org/10.1016/s0022-2143(99)90188-9.

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6

Li, Yi-Ping, та Michael B. Reid. "Effect of tumor necrosis factor-α on skeletal muscle metabolism". Current Opinion in Rheumatology 13, № 6 (2001): 483–87. http://dx.doi.org/10.1097/00002281-200111000-00005.

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7

Shiraki, Makoto, Yoichi Terakura, Junpei Iwasa та ін. "Elevated serum tumor necrosis factor-α and soluble tumor necrosis factor receptors correlate with aberrant energy metabolism in liver cirrhosis". Nutrition 26, № 3 (2010): 269–75. http://dx.doi.org/10.1016/j.nut.2009.04.016.

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8

Leeper-Woodford, S. K., and B. W. Tobin. "Tumor necrosis factor activity of pancreatic islets." American Journal of Physiology-Endocrinology and Metabolism 273, no. 2 (1997): E433—E437. http://dx.doi.org/10.1152/ajpendo.1997.273.2.e433.

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Tumor necrosis factor (TNF) is involved in the pathogenesis of acute sepsis-induced organ injury and has been implicated as a mediator of metabolic alterations observed during sepsis. Pancreatic islet cell function may be significantly compromised during sepsis or endotoxemia, and sepsis also increases plasma levels of epinephrine, a modifier of islet insulin secretion. We proposed that islets exposed to bacterial lipopolysaccharide (LPS) produce TNF and that epinephrine attenuates islet secretory activity. We monitored the effects of LPS and epinephrine on TNF and insulin activity of isolated

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9

Deuss, Ulrich, Massimo Buscema, Heike Schumacher та Werner Winkelmann. "In vitro effects of tumor necrosis factor-α on human thyroid follicular cells". Acta Endocrinologica 127, № 3 (1992): 220–25. http://dx.doi.org/10.1530/acta.0.1270220.

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Tumor necrosis factor-α is assumed to be an important mediator in thyroid autoimmunity. In the present study we have shown that human thyrocytes possess a single specific binding site for recombinant tumor necrosis factor-α with an average of 9,300 receptors/cell (Kd = 1.9 · 10−10 mol). The effects of the cytokine on thyroid cell proliferation were assessed by 3H-thymidine uptake as well as by the protein and DNA content of cell monolayers. Low dose tumor necrosis factor-α resulted in a moderate stimulation of cell proliferation with an increase of 3H-thymidine incorporation from 44,613±7,989

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10

Watanabe, Naoki, Naoki Tsuji, Yasushi Tsuji, et al. "Endogenous Tumor Necrosis Factor Inhibits the Cytotoxicity of Exogenous Tumor Necrosis Factor and Adriamycin in Pancreatic Carcinoma Cells." Pancreas 13, no. 4 (1996): 395–400. http://dx.doi.org/10.1097/00006676-199611000-00009.

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11

Cunnion, Kenji M. "Tumor Necrosis Factor Receptors Encoded by Poxviruses." Molecular Genetics and Metabolism 67, no. 4 (1999): 278–82. http://dx.doi.org/10.1006/mgme.1999.2878.

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12

Plomgaard, Peter, Christian P. Fischer, Tobias Ibfelt, Bente K. Pedersen та Gerrit van Hall. "Tumor Necrosis Factor-α Modulates Humanin VivoLipolysis". Journal of Clinical Endocrinology & Metabolism 93, № 2 (2008): 543–49. http://dx.doi.org/10.1210/jc.2007-1761.

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13

Matic, Maja, Beatrice Leveugle, and Howard M. Fillit. "Tumor Necrosis Factor-Alpha Alters the Metabolism of Endothelial Cell Proteoglycans." Autoimmunity 18, no. 4 (1994): 275–84. http://dx.doi.org/10.3109/08916939409009529.

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14

VAN LANSCHOT, J. J. B., K. MEALY, and D. W. WILMORE. "The Effects of Tumor Necrosis Factor on Intestinal Structure and Metabolism." Annals of Surgery 212, no. 6 (1990): 663–70. http://dx.doi.org/10.1097/00000658-199012000-00003.

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15

Firdaus, Muhamad, Fadhilah Purna Agustin, Alif J. Kholifatul, Nugroho Wiratama та Yusuf Adi Sudjatmiko. "ANTIOBESITY OF FUCOXANTHIN FROM Sargassumechinocarpum BY INCREASING β-OXIDATION IN ADIPOCYTE". KnE Life Sciences 2, № 1 (2015): 97. http://dx.doi.org/10.18502/kls.v1i0.91.

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Fucoxanthin is a one of carotenoids that contained in brown seaweeds. This compound has been affected to lipid metabolism. The aim of this study was to evaluate the antiobesity of fucoxanthin of Sargassumechinocarpum on adipocyte by increasing of adiponectin and decreasing of tumor necrosis factor a expressions. Fucoxanthin was isolated from Sargassumechinocarpum and validated by infrared spectrophotometer. Adipocyte was obtained from pre-adipocyte cell from viscera tissue of wistar rats (Rattusnorvegicus) and cultured in fetal bovine serum and Dulbeccos modified eagle’s medium. Adipocyte was

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16

Alferova, V. I., and S. V. Mustafina. "Adipocytokines Through the Prism of Human Metabolic Phenotypes." Doctor.Ru 22, no. 4 (2023): 18–23. http://dx.doi.org/10.31550/1727-2378-2023-22-4-18-23.

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Aim: To study the features of adiponectin, leptin, resistin, adipsin, interleukin 6, and tumor necrosis factor α levels in individuals with a metabolically healthy and unhealthy phenotype at different values of body weight according to the literature. Key points. The results of foreign and domestic studies of the levels of adipocytokines in metabolically healthy and unhealthy phenotypes in individuals with different body weights are presented. Adipokines such as adiponectin, leptin, resistin, adipsin, interleukin 6, and tumor necrosis factor α were analyzed. Data are given on the pathogenetic

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17

Shenglong, Ye, Tang Zhaoyou та Bruce R. Bistrian. "Tumor necrosis factor-α alters protein metabolism and cell-cycle kinetics in malignant tumor". Chinese Journal of Cancer Research 8, № 1 (1996): 19–22. http://dx.doi.org/10.1007/bf02674962.

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18

Kitaura, Hideki, Aseel Marahleh, Fumitoshi Ohori та ін. "Role of the Interaction of Tumor Necrosis Factor-α and Tumor Necrosis Factor Receptors 1 and 2 in Bone-Related Cells". International Journal of Molecular Sciences 23, № 3 (2022): 1481. http://dx.doi.org/10.3390/ijms23031481.

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Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine expressed by macrophages, monocytes, and T cells, and its expression is triggered by the immune system in response to pathogens and their products, such as endotoxins. TNF-α plays an important role in host defense by inducing inflammatory reactions such as phagocytes and cytocidal systems activation. TNF-α also plays an important role in bone metabolism and is associated with inflammatory bone diseases. TNF-α binds to two cell surface receptors, the 55kDa TNF receptor-1 (TNFR1) and the 75kDa TNF receptor-2 (TNFR2). Bone is in a constant

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19

MOCELLIN, S., C. ROSSI, P. PILATI, and D. NITTI. "Tumor necrosis factor, cancer and anticancer therapy." Cytokine & Growth Factor Reviews 16, no. 1 (2005): 35–53. http://dx.doi.org/10.1016/j.cytogfr.2004.11.001.

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20

Grunfeld, Carl, and Kenneth R. Feingold. "Tumor necrosis factor, cytokines, and the hyperlipidemia of infection." Trends in Endocrinology & Metabolism 2, no. 6 (1991): 213–19. http://dx.doi.org/10.1016/1043-2760(91)90027-k.

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21

Carroll, James L., Diann M. McCoy, Stephen E. McGowan, Ronald G. Salome, Alan J. Ryan та Rama K. Mallampalli. "Pulmonary-specific expression of tumor necrosis factor-α alters surfactant lipid metabolism". American Journal of Physiology-Lung Cellular and Molecular Physiology 282, № 4 (2002): L735—L742. http://dx.doi.org/10.1152/ajplung.00120.2001.

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Tumor necrosis factor (TNF)-α is a major cytokine implicated in inducing acute and chronic lung injury, conditions associated with surfactant phosphatidylcholine (PtdCho) deficiency. Acutely, TNF-α decreases PtdCho synthesis but stimulates surfactant secretion. To investigate chronic effects of TNF-α, we investigated PtdCho metabolism in a murine transgenic model exhibiting lung-specific TNF-α overexpression. Compared with controls, TNF-α transgenic mice exhibited a discordant pattern of PtdCho metabolism, with a decrease in PtdCho and disaturated PtdCho (DSPtdCho) content in the lung, but inc

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22

Yamada, Kentaro, Chizuko Inada, Shuichi Otabe, Naoko Takane, Hideki Hayashi, and Kyohei Nonaka. "Effects of free radical scavengers on cytokine actions on islet cells." Acta Endocrinologica 128, no. 4 (1993): 379–84. http://dx.doi.org/10.1530/acta.0.1280379.

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We investigated the effect of free radical scavengers on the actions of cytokines on islet cells. Interferon-γ and tumor necrosis factor-α reduced the nicotinamide adenine dinucleotide content of mouse islet cells; the combination of interferon-γ (4×105 U/I) and tumor necrosis factor-α (4×105 U/I) caused nicotinamide adenine dinucleotide reduction by ∼40%. Dimethyl urea and dimethyl sulfoxide prevented the decrease, whereas superoxide dismutase, catalase, and mannitol were not effective. Dimethyl urea and dimethyl sulfoxide protected islet cells from the synergistic cytotoxic action of interfe

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23

She, Z. W., M. D. Wewers, D. J. Herzyk, A. L. Sagone, and W. B. Davis. "Tumor necrosis factor primes neutrophils for hypochlorous acid production." American Journal of Physiology-Lung Cellular and Molecular Physiology 257, no. 6 (1989): L338—L345. http://dx.doi.org/10.1152/ajplung.1989.257.6.l338.

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Tumor necrosis factor (TNF) has a weak direct effect on neutrophil oxidative metabolism and primes neutrophils for oxidant release in response to other stimuli. We examined the effect of recombinant human TNF alpha (rTNF alpha) on production of hypochlorous acid (HOCl) by human neutrophils. TNF alone, even at concentrations of 1,000 U/ml, did not stimulate HOCl production. In contrast, rTNF alpha, in a dose-dependent manner, primed neutrophils for HOCl production in response to the weak agent unopsonized zymosan. rTNF alpha concentrations as low as 10 U/ml resulted in a fivefold increase in HO

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24

Chang, I., S. Kim, J. Y. Kim, et al. "Nuclear Factor B Protects Pancreatic -Cells From Tumor Necrosis Factor- -Mediated Apoptosis." Diabetes 52, no. 5 (2003): 1169–75. http://dx.doi.org/10.2337/diabetes.52.5.1169.

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25

Evans, D. A., D. O. Jacobs, and D. W. Wilmore. "Effects of tumour necrosis factor on protein metabolism." British Journal of Surgery 80, no. 8 (1993): 1019–23. http://dx.doi.org/10.1002/bjs.1800800830.

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26

Wan, J. M., F. Fogt, B. R. Bistrian, and N. W. Istfan. "Evaluation of antitumor effect of tumor necrosis factor in terms of protein metabolism and cell cycle kinetics." American Journal of Physiology-Cell Physiology 265, no. 2 (1993): C365—C374. http://dx.doi.org/10.1152/ajpcell.1993.265.2.c365.

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To determine the significance of protein breakdown in regulating tumor growth and to better understand the antitumor mechanism of tumor necrosis factor in vivo, we measured the effects of a 6-h constant intravenous infusion of human recombinant tumor necrosis factor-alpha (rHuTNF) on tumor protein metabolism and cell cycle kinetics in rats bearing the Walker-256 carcinosarcoma. Protein metabolism was investigated with the use of [14C]leucine infusion; estimates of tumor cell cycle kinetics were obtained in vivo by use of 5-bromo-2'-deoxyuridine (BrdUrd) pulse labeling and bivariate BrdUrd/DNA

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27

Tereshchenko, I. V., та P. E. Kayushev. "Tumor necrosis factor α and its role in pathologies". Russian Medical Inquiry 6, № 9 (2022): 523–27. http://dx.doi.org/10.32364/2587-6821-2022-6-9-523-527.

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Over the past years, the views on the role played by tumor necrosis factor α (TNF-α) in the body have changed. The aim of this review is to provide updates on TNF-α functions in various pathological conditions. While working on the review, the authors made search and analysis of full-text reviews and original articles in foreign (English) and Russian languages using such databases as eLIBRARY.RU, Google Scholar, Web of Science, Scopus and PubMed, mostly from 2018–2022. A priority was given to the original publications. TNF-α is a multifunctional pro-inflammatory cytokine which stimulates the p

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28

Tredget, E. E., Y. M. Yu, S. Zhong, et al. "Role of interleukin 1 and tumor necrosis factor on energy metabolism in rabbits." American Journal of Physiology-Endocrinology and Metabolism 255, no. 6 (1988): E760—E768. http://dx.doi.org/10.1152/ajpendo.1988.255.6.e760.

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A study of the combined effects of intravenous infusion of the recombinant cytokines beta-interleukin 1 (IL-1) and alpha-tumor necrosis factor (TNF) on energy substrate metabolism in awake, conditioned, adult rabbits was performed. After a 2-h basal or control period, 48-h fasted rabbits were administered TNF and IL-1 as a bolus (5 micrograms/kg) followed by a continuous intravenous infusion (25 ng.kg-1.min-1) for 3 h. Significant increases in plasma lactate (P less than 0.01), glucose (P less than 0.01), and triglycerides (P less than 0.05) occurred during the combined infusion of IL-1 and TN

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29

Prins, Johannes B., Carola U. Niesler, Clay M. Winterford та ін. "Tumor Necrosis Factor-α Induces Apoptosis of Human Adipose Cells". Diabetes 46, № 12 (1997): 1939–44. http://dx.doi.org/10.2337/diab.46.12.1939.

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30

Karnes, Jonathan M., Scott D. Daffner, and Colleen M. Watkins. "Multiple roles of tumor necrosis factor-alpha in fracture healing." Bone 78 (September 2015): 87–93. http://dx.doi.org/10.1016/j.bone.2015.05.001.

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31

Prins, J. B., C. U. Niesler, C. M. Winterford, et al. "Tumor necrosis factor-alpha induces apoptosis of human adipose cells." Diabetes 46, no. 12 (1997): 1939–44. http://dx.doi.org/10.2337/diabetes.46.12.1939.

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32

Gulick, T., M. K. Chung, S. J. Pieper, L. G. Lange, and G. F. Schreiner. "Interleukin 1 and tumor necrosis factor inhibit cardiac myocyte beta-adrenergic responsiveness." Proceedings of the National Academy of Sciences 86, no. 17 (1989): 6753–57. http://dx.doi.org/10.1073/pnas.86.17.6753.

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Reversible congestive heart failure can accompany cardiac allograft rejection and inflammatory myocarditis, conditions associated with an immune cell infiltrate of the myocardium. To determine whether immune cell secretory products alter cardiac muscle metabolism without cytotoxicity, we cultured cardiac myocytes in the presence of culture supernatants from activated immune cells. We observed that these culture supernatants inhibit beta-adrenergic agonist-mediated increases in cultured cardiac myocyte contractility and intracellular cAMP accumulation. The myocyte contractile response to increa

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33

Ohashi, K. "Tumor necrosis factor-alpha inhibits human chorionic gonadotropin secretion." Journal of Clinical Endocrinology & Metabolism 74, no. 1 (1992): 130–34. http://dx.doi.org/10.1210/jc.74.1.130.

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34

Badenhoop, K. "Tumor necrosis factor beta gene polymorphisms in Graves' disease." Journal of Clinical Endocrinology & Metabolism 74, no. 2 (1992): 287–91. http://dx.doi.org/10.1210/jc.74.2.287.

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35

OZAWA, MINORU, KANJI SATO, DOO CHOL HAN, MASANOBU KAWAKAMI, TOSHIO TSUSHIMA та KAZUO SHIZUME. "Effects of Tumor Necrosis Factor-α/Cachectin on Thyroid Hormone Metabolism in Mice*". Endocrinology 123, № 3 (1988): 1461–67. http://dx.doi.org/10.1210/endo-123-3-1461.

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36

BEUTLER, BRUCE, and ANTHONY CERAMI. "Cachectin (Tumor Necrosis Factor): A Macrophage Hormone Governing Cellular Metabolism and Inflammatory Response." Endocrine Reviews 9, no. 1 (1988): 57–66. http://dx.doi.org/10.1210/edrv-9-1-57.

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37

Zhang, Wenyu, and Rosemary Dziak. "Tumor necrosis factor alpha stimulates arachidonic acid metabolism in human osteoblastic osteosarcomal cells." Prostaglandins, Leukotrienes and Essential Fatty Acids 54, no. 6 (1996): 427–31. http://dx.doi.org/10.1016/s0952-3278(96)90026-5.

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38

Royall, James A., Paula D. Gwin, Dale A. Parks та Bruce A. Freeman. "Responses of vascular endothelial oxidant metabolism to lipopolysaccharide and tumor necrosis factor-α". Archives of Biochemistry and Biophysics 294, № 2 (1992): 686–94. http://dx.doi.org/10.1016/0003-9861(92)90742-f.

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39

Kovács, P., L. Köhidai та G. Csaba. "Effects of tumor necrosis factor α (TNFα) on the phospholipid metabolism ofTetrahymena pyriformis". Cell Biochemistry and Function 16, № 2 (1998): 87–97. http://dx.doi.org/10.1002/(sici)1099-0844(199806)16:2<87::aid-cbf770>3.0.co;2-i.

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40

Ghezzi, Pietro, Beatrice Saccardo, and Marina Bianchi. "Recombinant tumor necrosis factor depresses cytochrome P450-dependent microsomal drug metabolism in mice." Biochemical and Biophysical Research Communications 136, no. 1 (1986): 316–21. http://dx.doi.org/10.1016/0006-291x(86)90912-5.

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41

Goodman, M. N. "Tumor necrosis factor induces skeletal muscle protein breakdown in rats." American Journal of Physiology-Endocrinology and Metabolism 260, no. 5 (1991): E727—E730. http://dx.doi.org/10.1152/ajpendo.1991.260.5.e727.

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The metabolic response to infection includes loss of lean tissue and increased nitrogen excretion. The loss of muscle tissue during infection results in large part from accelerated skeletal muscle protein breakdown. Recent studies suggest that macrophage-derived products secreted during infection may signal increased muscle proteolysis. To test this, in the present report the ability of interleukin (IL-1) and tumor necrosis factor (TNF) to enhance muscle proteolysis was examined. Young rats were injected intravenously with either recombinant human IL-1 or TNF. For comparison some rats were inj

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42

Barnawi, Amnah I., Mohamad H. Qari, Khalid O. Abulnaja, and Shaker A. Mousa. "Correlation Between the Frequency of Painful Crises in Sickle Cell Anemia and the Biomarkers of Inflammation, Endothelial Dysfunction, Coagulation Activation and Bone Metabolism." Saudi Journal of Internal Medicine 7, no. 2 (2017): 11–19. http://dx.doi.org/10.32790/sjim.2017.7.2.3.

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Objective: Sickle cell anemia is a widespread inherited hemolytic anemia, characterized by chronic hemolysis, infections, recurrent occlusion of the microcirculation and painful crises. In this cross-sectional study, we investigated the correlation between biomarkers of inflammation, endothelial dysfunction, coagulation activation and bone metabolism, with the frequency of painful crisis in sickle cell anemia adult patients, to understand the potential role of these biomarkers in the management of sickle cell anemia. Methods: Sixty-three sickle cell anemia patients were enrolled in this

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43

Bo, S., A. Signorile, G. Menato та ін. "C-reactive protein and tumor necrosis factor-α in gestational hyperglycemia". Journal of Endocrinological Investigation 28, № 11 (2005): 779–86. http://dx.doi.org/10.1007/bf03347566.

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44

Mondon, Carl E., and H. Fletcher Starnes. "Differential metabolic responses to tumor necrosis factor with increase in age." Metabolism 41, no. 9 (1992): 970–81. http://dx.doi.org/10.1016/0026-0495(92)90123-r.

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45

Hivert, Marie-France, Lisa M. Sullivan, Peter Shrader та ін. "The association of tumor necrosis factor α receptor 2 and tumor necrosis factor α with insulin resistance and the influence of adipose tissue biomarkers in humans". Metabolism 59, № 4 (2010): 540–46. http://dx.doi.org/10.1016/j.metabol.2009.08.017.

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46

Chang, Ming-Chu, Yu-Ting Chang, Yu-Wen Tien, Po-Chin Liang, Shu-Chen Wei, and Jau-Min Wong. "ASSOCIATION OF TUMOR NECROSIS FACTOR - PROMOTER HAPLOTYPE WITH CHRONIC PANCREATITIS." Pancreas 33, no. 4 (2006): 451. http://dx.doi.org/10.1097/00006676-200611000-00055.

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47

Pohanka, Miroslav, Branislav Ruttkay-Nedecký, Josef Fusek, Vojtěch Adam, and René Kizek. "Melatonin Regulates Oxidative Stress Initiated by Freund’s Complete Adjuvant." Acta Medica (Hradec Kralove, Czech Republic) 58, no. 1 (2015): 21–24. http://dx.doi.org/10.14712/18059694.2015.87.

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Melatonin is a hormone with strong antioxidant properties. In this experiment, Freund’s complete adjuvant was used as a stressogenic substance given to laboratory outbred mice, whereas melatonin was investigated as a protectant against the stressogenic effect. Levels of low molecular weight antioxidants, thiobarbituric acid reactive substances, and tumor necrosis factor α and activity of glutathione reductase were determined in blood from the animals. Surprisingly, melatonin was not involved in direct regulation of antioxidants, thiobarbituric acid reactive substances and tumor necrosis factor

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48

Kondratieva, L. V., T. V. Popkova, and E. L. Nasonov. "Influence of biologics on carbohydrate metabolism and risk of diabetes." Rheumatology Science and Practice 57, no. 2 (2019): 222–28. http://dx.doi.org/10.14412/1995-4484-2019-222-228.

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In the article the analysis of the literature on the impact of biologics of different groups (inhibitors of tumor necrosis factor α, tocilizumab, abatacept, rituximab and interleukin 1 inhibitors) on the production of insulin by the pancreas, insulin resistance and the risk of development of the 2nd type diabetes in patients with rheumatic diseases.

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49

Nagano, Kenichi, Neil Alles, Anower Hussain Mian та ін. "The tumor necrosis factor type 2 receptor plays a protective role in tumor necrosis factor-α-induced bone resorption lacunae on mouse calvariae". Journal of Bone and Mineral Metabolism 29, № 6 (2011): 671–81. http://dx.doi.org/10.1007/s00774-011-0270-z.

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50

Puimège, Leen, Claude Libert, and Filip Van Hauwermeiren. "Regulation and dysregulation of tumor necrosis factor receptor-1." Cytokine & Growth Factor Reviews 25, no. 3 (2014): 285–300. http://dx.doi.org/10.1016/j.cytogfr.2014.03.004.

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