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Sickness-associated anorexia : mother nature’s idea of immunonutrition?

dc.contributor.authorVan Niekerk, Gustaven_ZA
dc.contributor.authorIsaacs, Ashwin W.en_ZA
dc.contributor.authorNell, Theo A.en_ZA
dc.contributor.authorEngelbrecht, Anna-Marten_ZA
dc.date.accessioned2016-07-11T10:26:41Z
dc.date.available2016-07-11T10:26:41Z
dc.date.issued2016
dc.identifier.citationVan Niekerk, G, et al. 2016. Sickness-associated anorexia : mother nature’s idea of immunonutrition?. Mediators of Inflammation, 2016 (Article ID 8071539), doi: http://dx.doi.org/10.1155/2016/8071539
dc.identifier.issn1466-1861 (online)
dc.identifier.issn0962-9351 (print)
dc.identifier.otherdoi: http://dx.doi.org/10.1155/2016/8071539
dc.identifier.urihttp://hdl.handle.net/10019.1/99121
dc.descriptionCITATION: Van Niekerk, G, et al. 2016. Sickness-associated anorexia : mother nature’s idea of immunonutrition?. Mediators of Inflammation, 2016 (Article ID 8071539), doi: http://dx.doi.org/10.1155/2016/8071539.
dc.descriptionThe original publication is available at http://www.hindawi.com
dc.descriptionPublication of this article was funded by the Stellenbosch University Open Access Fund.
dc.description.abstractDuring an infection, expansion of immune cells, assembly of antibodies, and the induction of a febrile response collectively place continual metabolic strain on the host. These considerations also provide a rationale for nutritional support in critically ill patients. Yet, results from clinical and preclinical studies indicate that aggressive nutritional support does not always benefit patients and may occasionally be detrimental. Moreover, both vertebrates and invertebrates exhibit a decrease in appetite during an infection, indicating that such sickness-associated anorexia (SAA) is evolutionarily conserved. It also suggests that SAA performs a vital function during an infection. We review evidence signifying that SAA may present a mechanism by which autophagic flux is upregulated systemically. A decrease in serum amino acids during an infection promotes autophagy not only in immune cells, but also in nonimmune cells. Similarly, bile acids reabsorbed postprandially inhibit hepatic autophagy by binding to farnesoid X receptors, indicating that SAA may be an attempt to conserve autophagy. In addition, augmented autophagic responses may play a critical role in clearing pathogens (xenophagy), in the presentation of epitopes in nonprovisional antigen presenting cells and the removal of damaged proteins and organelles. Collectively, these observations suggest that some patients might benefit from permissive underfeeding.en_ZA
dc.format.extent12 pages
dc.language.isoen_ZAen_ZA
dc.publisherHindawi Publishing Corporation
dc.subjectAnorexia nervosaen_ZA
dc.subjectEating disordersen_ZA
dc.subjectImmune systemen_ZA
dc.subjectNutritionen_ZA
dc.titleSickness-associated anorexia : mother nature’s idea of immunonutrition?en_ZA
dc.typeArticleen_ZA
dc.description.versionPublisher's version
dc.rights.holderAuthors retain copyright


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