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dc.contributor.authorLobo, Julie Calixto-
dc.contributor.authorAranha, Luciana Nicolau-
dc.contributor.authorMoraes, Cristiane-
dc.contributor.authorBrito, Luciana Catunda-
dc.contributor.authorMafra, Denise-
dc.date.accessioned2021-11-25T17:14:16Z-
dc.date.available2021-11-25T17:14:16Z-
dc.date.issued2011-
dc.identifier.citationLOBO, Julie Calixto et al. Linking Zinc and Leptin in Chronic Kidney Disease: Future Directions. Biological Trace Element Research, [s. l.], v. 146, n. 1, p. 1-5, 2011.pt_BR
dc.identifier.urihttp://www.repositorio.ufc.br/handle/riufc/62483-
dc.language.isopt_BRpt_BR
dc.publisherBiological Trace Element Researchpt_BR
dc.subjectLeptinpt_BR
dc.subjectZincpt_BR
dc.subjectAnorexiapt_BR
dc.subjectChronic kidney diseasept_BR
dc.titleLinking Zinc and Leptin in Chronic Kidney Disease: Future Directionspt_BR
dc.typeArtigo de Periódicopt_BR
dc.description.abstract-ptbrAnorexia is a common complication in patients with chronic kidney disease (CKD) and is associated with the development of malnutrition and an increased risk of mortality. Several compounds are linked to anorexia in these patients; however, the mechanisms are unknown. Zinc (Zn) deficiency is associated with decreased food intake and has been observed in CKD patients. In addition, leptin is an anorexigenic peptide, and patients with CKD present generally high levels of this hormone. Studies have suggested an association between Zn and leptin status in human and rats; however, the results are inconsistent. Some claimed that Zn supplementation does not change leptin release or that there is no significant relationship between Zn and leptin. Others have reported that Zn might be a mediator of leptin production. CKD patients have hyperleptinemia and hypozincemia, but the relationship between Zn deficiency and leptin levels in CKD patients has been poorly understood until now. The aim of this review is to integrate knowledge on leptin and Zn actions to provide a cohesive clinical perspective regarding their interactions in CKD patientspt_BR
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