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Relationship of food intake, body composition, and tumor growth to host metabolism in nongrowing mice with sarcoma.
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1980
Year
NutritionFood IntakePathologyExperimental NutritionTumor BiologyBody CompositionSpontaneous Food IntakeMolecular NutritionCancer MetabolismRadiation OncologyMetabolic StateCancer ResearchTumor-bearing AnimalsAnimal PhysiologyHealth SciencesNutrient PhysiologyCellular NutritionAnimal NutritionTumor GrowthClinical NutritionPharmacologyEnergy MetabolismPhysiologyMetabolismMedicine
Abstract A methylcholanthrene-induced sarcoma was transplanted in adult weight-stable mice. The relationship between spontaneous food intake and tumor growth, body composition, and host metabolism was studied. Tumor-bearing animals decreased their spontaneous food intake gradually from the day when the tumor became palpable (5 to 7 days) until reaching 50 to 60% of their initial intake 7 to 8 days later. The body dry weight (including tumor) and the lipid content of the tumor-bearing animals decreased significantly. This decrease in body dry weight was determined primarily by the loss of lipids. However, pair-fed animals maintained their lean body mass as well as their body lipids, indicating that decreased energy intake because of anorexia cannot be the cause of tissue depletion of the tumor host. The tumor-bearing animals as well as the pair-fed controls seemed to be in a positive nitrogen balance due to decreased urinary excretion of urea. This indicates that catabolism of amino acids was decreased in both tumor-bearing animals and pair-fed controls. However, the urea cycle activity in tumor-influenced liver was unaltered as determined in vitro. The nitrogen and carbon atoms in the tumor tissue originated from food and from the carcass tissues. The breakdown of skeletal muscle supplied approximately 50% of the tumor tissue, while the food and other host tissues supplied the rest. The energy demand for tumor growth and for nitrogen and carbon translocation was also met by decreased urea cycle activity and by increased glucose uptake in the liver concomitant with increased gluconeogenesis. The hepatic incorporation rate of [14C]glucose into carbondioxide in vitro was doubled in tumor-bearing animals but unchanged in pair-fed controls. The hepatic oxidation rate of [14C]palmitate in vitro was decreased in tumor-bearing animals, while the oxidation rate of 14C-labeled amino acids was unchanged. Tumor-bearing animals decreased the excretion of sodium and potassium, while pair-fed controls excreted these ions at control levels. The results show that several well-known metabolic alterations in the tumor host cannot be explained by the decreased intake of food only.