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Ácido eicosapentanóico no tratamento da caquexia neoplásica : monografia : Eicosapentaenoic acid in the treatment of cancer cachexia
| Summary: | Thesis abstract: Cancer cachexia occurs in about 80% of cancer patients, and it’s a major contributor to the morbidity and mortality in these patients. The cachexia syndrome is complex and difficult to define, and is characterized by the presence of anorexia, hypermetabolism, extensive loss of adipose tissue and skeletal muscle, chronic inflammation and marked metabolic changes.It reflects a catabolic metabolism induced by an abnormal reponse to the tumor presence. While anorexia is present in this syndrome, the protein-energy deficit alone does not explain the pathogenesis of cachexia. The mediators responsible for all these metabolic changes are thought to be host and tumor derived, and include proinflammatory cytokines, the neuroendocrine system,and certain tumor specific factors such as proteolysis inducing factor (PIF) and lipid mobilizing factor (LMF). The presence of an acute phase response as been linked to accelerated weight loss, and is thought to be initiated by cytokines like interleukin (IL)-6 e IL-8, production of which is induced by PIF. The loss of adipose tissue is linked to increased triglycerides degradation, rather than a decrease in its synthesis. This process is a result of the presence of LMF, which stimulates lipolysis through a cAMP mediated pathway via interaction with β-adrenergic receptors. Loss of skeletal muscle arises from both a reduction in protein synthesis and an increase in protein degradation. The major proteolytic pathway involved in protein breakdown is the ATP-ubiquitinproteassome dependent pathway, whose expression is enhanced by the presence of PIF and tumor necrosis factor (TNF)-α. (...) |
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| Subject: | Ciências da Nutrição--Tese de licenciatura Alterações do Peso Corporal Universidade do Porto, Faculdade de Ciências da Nutrição e Alimentação, Licenciatura em Ciências da Nutrição--Dissertações Suplementação Dietética Áreas de estágio--Nutrição Clínica--Nutrição Comunitária (Saúde Pública)--Restauração e Alimentação Colectiva--Relatório de estágio Neoplasias |
| Country: | Portugal |
| Document type: | other |
| Access type: | Open |
| Associated institution: | Repositório Aberto da Universidade do Porto |
| Language: | Portuguese |
| Origin: | Repositório Aberto da Universidade do Porto |
| Summary: | Thesis abstract: Cancer cachexia occurs in about 80% of cancer patients, and it’s a major contributor to the morbidity and mortality in these patients. The cachexia syndrome is complex and difficult to define, and is characterized by the presence of anorexia, hypermetabolism, extensive loss of adipose tissue and skeletal muscle, chronic inflammation and marked metabolic changes.It reflects a catabolic metabolism induced by an abnormal reponse to the tumor presence. While anorexia is present in this syndrome, the protein-energy deficit alone does not explain the pathogenesis of cachexia. The mediators responsible for all these metabolic changes are thought to be host and tumor derived, and include proinflammatory cytokines, the neuroendocrine system,and certain tumor specific factors such as proteolysis inducing factor (PIF) and lipid mobilizing factor (LMF). The presence of an acute phase response as been linked to accelerated weight loss, and is thought to be initiated by cytokines like interleukin (IL)-6 e IL-8, production of which is induced by PIF. The loss of adipose tissue is linked to increased triglycerides degradation, rather than a decrease in its synthesis. This process is a result of the presence of LMF, which stimulates lipolysis through a cAMP mediated pathway via interaction with β-adrenergic receptors. Loss of skeletal muscle arises from both a reduction in protein synthesis and an increase in protein degradation. The major proteolytic pathway involved in protein breakdown is the ATP-ubiquitinproteassome dependent pathway, whose expression is enhanced by the presence of PIF and tumor necrosis factor (TNF)-α. (...) |
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