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Abnormal substrate metabolism and
nutritional strategies in cancer management
Rossi-Fanelli F, Cascino A, Muscaritoli M
III Department of Internal Medicine, University La Sapienza,
Rome, Italy
Impairment of the nutritional
state plays a major role in the morbidity and mortality of cancer
patients.
However, the opportunity of providing artificial nutritional support to these
patients is still debated, because of the concern that energy substrates
administered to replete the host may concomitantly stimulate tumor growth.
A correct nutritional approach to cancer patients should thus be based on a
thorough knowledge of both host and tumor metabolic needs and host-tumor
metabolic interactions.
Specific modifications of plasma levels of glucogenic, aromatic,
sulfur-containing and branched-chain amino acids have been demonstrated in
cancer patients, indicating a specific influence of the tumor on amino acid
metabolism.
Little is known about protein metabolism in neoplastic tissue.
Interference with tumor growth has been attempted by deprivation of single amino
acids with controversial results.
Increased gluconeogenesis and insulin resistance are responsible for the two
main abnormalities in carbohydrate metabolism in cancer patients, namely
increased glucose turnover and impaired glucose tissue disposal.
Lipid metabolism is also affected by the neoplasm: soluble factors such as
"lipid-mobilizing factor" lead to increased fat mobilization from
adipose tissue; plasma elimination of exogenous triglycerides has also been
found to be reduced probably because of a tumor-related decrease in lipoprotein
lipase activity.
The differences in glucose and fat utilization between tumor and host should be
considered in the nutritional approach to cancer patients.
Data in this respect are controversial and have been obtained only in
experimental animals.
(ABSTRACT TRUNCATED AT 250 WORDS)
PMID:
1766060 [PubMed - indexed for MEDLINE]
Source: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1766060&dopt=Abstract
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