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Glucose dynamics, energy metabolism, and nitrogen balance were studied in eight malnourished cancer patients and seven malnourished patients without cancer. Glucose flux was measured by single injection of [6-3H]glucose and [U-14C]glucose. Energy expenditure was measured by indirect calorimetry. Each patient was studied after an overnight fast and during constant gastric infusion of a formula diet. Cancer patients had elevated glucose flux when fasting, corresponding to 42% of their spontaneous daily intake of glucose. At least one-half of the elevated flux in cancer patients compared with controls was due to increased recycling of glucose carbon after an overnight fast. Feeding doubled the total glucose flux in both cancer and control patients. The recycling was unchanged in the cancer group and disappeared in the controls during feeding. The increased glucose flux in cancer patients was concomitant with normal resting energy expenditure during periods of both fasting and feeding. Glucose flux in relation to energy expenditure was doubled in cancer patients compared to controls, and the glucose flux in fed cancer patients was similar to the rate of glucose infusion, which shows that the endogenous production of glucose was not inhibited. Cancer and control patients reached a comparable positive energy and nitrogen balance, allowing for their overall caloric intake. Our results show that cancer patients seem to have a characteristically increased glucose demand, which contributes to their weight loss when fasting. The energy drain by this elevated glucose flux can explain, as a maximum estimate, a loss of about 0.9 kg of body fat per 30-day period.

Reutilization of amino acid carbons was evaluated in relation to increased turnover of albumin in tumor-bearing mice. A methylcholanthrene-induced sarcoma (MCG 101) was used in nongrowing mice (C57BL/6J). Sarcoma-bearing mice developed hypoalbuminemia, but pair-fed controls did not. The hypoalbuminemia was caused by increased albumin degradation rate, measured by injection of Na214CO3, and by exponentially increased deposition of albumin into the tumor compartment. The fractional synthesis rate of albumin was doubled in tumor-bearing mice compared with controls. The translational capacity of albumin synthesis evaluated in vitro was maintained in tumor host livers. The recycling of [14C]leucine carbons was almost extinguished in plasma albumin of sarcoma-bearing mice, while that of control mice contributed to 30 to 40% of the total leucine carbon flux in turned over albumin. The recycling of arginine carbons was also different when measured after simultaneous injection of [guanido-14C]arginine and [2,3-3H]arginine. The hepatic pool of free leucine was increased by 22% in tumor-bearing mice. It is concluded that increased albumin degradation in cancer may be a disordered event and is earlier and of initially greater quantitative importance than is altered synthesis of albumin for the development of hypoalbuminemia in experimental cancer.