The presence of cachexia as defined by a series of clinical symptoms, such as anorexia, weight loss, muscular atrophy, tissue wasting, altered organ function, is frequently observed in cancer and makes a decisive contribution to morbidity and mortality. The onset of neoplastic cachexia is characterized by two events: the presence of primary or secondary anorexia and alterations of the host's intermediate metabolism. Among the most frequent metabolic alterations described in cancer patients is an absolute or relative increase in basal energy consumption with lack of adaptation to fasting. The causes of increased energy consumption in cancer patients are still not clear. Numerous studies on glucose, fat and protein metabolism induced by cancer have significantly contributed to our understanding of the phenomenon. The main alterations of the glucose metabolism are increased glucose turnover and reduced peripheral utilization, both of which probably depend on the presence of the tumour, as shown by their normalization after treatment. Increased gluconeogenesis, from lactate and from gluconeogenetic AA, is the main factor responsible for increased glucose turnover. The main alterations of the fat metabolism are increased mobilization of lipids from adipose tissues, reduced use of exogenous triglycerides and increased oxidation of free fatty acids that cannot be suppressed by glucose. The main alterations of protein metabolism are increased protein turnover with reduced synthesis and increased degradation of muscular proteins and increased hepatic protein synthesis. Knowledge of the pathogenesis of neoplastic cachexia represents a valuable aid for its effective prevention and treatment.

[Energy metabolism in cancer patients] / G. F., Torelli; Cascino, Antonia; Muscaritoli, Maurizio; M., Russo; C., Falcone; S., Cherubini; ROSSI FANELLI, Filippo. - In: MINERVA GASTROENTEROLOGICA E DIETOLOGICA. - ISSN 1121-421X. - 43:4(1997), pp. 183-188.

[Energy metabolism in cancer patients].

CASCINO, Antonia;MUSCARITOLI, Maurizio;ROSSI FANELLI, Filippo
1997

Abstract

The presence of cachexia as defined by a series of clinical symptoms, such as anorexia, weight loss, muscular atrophy, tissue wasting, altered organ function, is frequently observed in cancer and makes a decisive contribution to morbidity and mortality. The onset of neoplastic cachexia is characterized by two events: the presence of primary or secondary anorexia and alterations of the host's intermediate metabolism. Among the most frequent metabolic alterations described in cancer patients is an absolute or relative increase in basal energy consumption with lack of adaptation to fasting. The causes of increased energy consumption in cancer patients are still not clear. Numerous studies on glucose, fat and protein metabolism induced by cancer have significantly contributed to our understanding of the phenomenon. The main alterations of the glucose metabolism are increased glucose turnover and reduced peripheral utilization, both of which probably depend on the presence of the tumour, as shown by their normalization after treatment. Increased gluconeogenesis, from lactate and from gluconeogenetic AA, is the main factor responsible for increased glucose turnover. The main alterations of the fat metabolism are increased mobilization of lipids from adipose tissues, reduced use of exogenous triglycerides and increased oxidation of free fatty acids that cannot be suppressed by glucose. The main alterations of protein metabolism are increased protein turnover with reduced synthesis and increased degradation of muscular proteins and increased hepatic protein synthesis. Knowledge of the pathogenesis of neoplastic cachexia represents a valuable aid for its effective prevention and treatment.
1997
01 Pubblicazione su rivista::01a Articolo in rivista
[Energy metabolism in cancer patients] / G. F., Torelli; Cascino, Antonia; Muscaritoli, Maurizio; M., Russo; C., Falcone; S., Cherubini; ROSSI FANELLI, Filippo. - In: MINERVA GASTROENTEROLOGICA E DIETOLOGICA. - ISSN 1121-421X. - 43:4(1997), pp. 183-188.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/457795
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