Abstract
Tissue damage is a threat to well-being because it is self-promoting; that is, hydrolases released from inflammatory or injured cells cause further injury and provide substrate for formation and propagation of free radicals. For this reason, the body must localise and limit the injury and clear tissue debris. To perform these functions, the organism has developed an acute-phase response that includes stereotyped, coordinated adaptations ranging from behavioural to physiological [1]. The acute-phase response includes the hepatic synthesis of large quantities of proteins. The functions of the acute-phase proteins vary widely and include binding proteins (opsonins), protease inhibitors, complement factors, apoproteins, fibrinogen, and others.
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References
Kushner I (1993) Regulation of the acute phase response by cytokines. Perspect Biol Med 36:611–622
Gotschlich EC (1989) C-reactive protein. A historical overview. Ann NY Acad Sci 557:9–18
Mitch WE, Goldberg AL (1996) Mechanisms of muscle wasting. The role of the ubiquitin-proteasome pathway. N Engl J Med 335:1897–1905
Feingold KR, Soued M, Serio MK et al (1989) Multiple cytokines stimulate hepatic lipid synthesis in vivo. Endocrinology 125:267–274
Beutler B, Greenwald D, Hulmes JD et al (1985) Identity of tumour necrosis factor and the macrophage-secreted factor cachectin. Nature 316:552–554
Baracos V, Rodemann HP, Dinarello CA et al (1983) Stimulation of muscle protein degradation and prostaglandin E2 release by leukocytic pyrogen (interleukin-1). N Engl J Med 308:553–558
Powanda MC, Beisel WR (1982) Hypothesis: leukocyte endogenous mediator/endogenous pyrogen/lymphocyte-activating factor modulates the development of nonspecific and specific immunity and affects nutritional status. Am J Clin Nutr 35:762–768
Norton JA, Moley JF, Green MV et al (1985) Parabiotic transfer of cancer anorexia/cachexia in male rats. Cancer Res 45:5547–5552
Tracey KJ, Morgello S, Koplin B et al (1990) Metabolic effects of cachectin/tumor necrosis factor are modified by site of production. Cachectin/tumor necrosis factor-secreting tumor in skeletal muscle induces chromic cachexia, while implantation in brain induces predominantly acute anorexia. J Clin Invest 86:2014–2024
Leibel RL, Rosenbaum M, Hirsch J (1995) Changes in energy expenditure resulting from altered body weight. N Engl J Med 332:621–628
Grunfeld C, Pang M, Shigenaga JK et al (1996) Serum leptin levels in the acquired immunodeficiency syndrome. J Clin Endocrinol Metab 81:4342–4346
Simons JP, Schols AM, Campfield LA et al (1997) Plasma concentration of total leptin and human lung-cancer-associated cachexia. Clin Sci (Colch) 93:273–277
Wallace AM, Sattar N, McMillan DC (1998) Effect of weight loss and the inflammatory response on leptin concentrations in gastrointestinal cancer patients. Clin Cancer Res 4:2977–2979
Takabatake N, Nakamura H, Abe S et al (1999) Circulating leptin in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 159:1215–1219
Schols AM, Creutzberg EC, Buurman WA et al (1999) Plasma leptin is related to proinflammatory status and dietary intake in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 160:1220–1226
Kaibara A, Moshyedi A, Auffenberg T et al (1998) Leptin produces anorexia and weight loss without inducing an acute phase response or protein wasting. Am J Physiol 274:R1518–R1525
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© 2006 Springer-Verlag Italia
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Mantovani, G. (2006). Cytokines in Cachexia. In: Mantovani, G., et al. Cachexia and Wasting: A Modern Approach. Springer, Milano. https://doi.org/10.1007/978-88-470-0552-5_21
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DOI: https://doi.org/10.1007/978-88-470-0552-5_21
Publisher Name: Springer, Milano
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