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Alterations in postprandial glycogen and lipid synthesis in cachectic tumor-bearing rats.

Alterations in the postprandial metabolism of glucose were investigated in groups of tumor-bearing rats and freely fed controls and in groups of normal rats whose food intake had been restricted to match that of the tumor-bearing rats. A standard mixed meal was administered by gavage, and the rate of incorporation of 3H from 3H2O into hepatic glycogen and into saponifiable lipids in the liver and adipose tissue was measured at intervals up to three hours after the meal. In tumor-bearing rats, the rate of glycogen synthesis rose by more than twice as much as normal after the meal, while the normal rise in rates of fatty acid synthesis was suppressed. In contrast, in the rats whose food intake had been restricted, the postprandial rise in hepatic glycogenesis was suppressed and the rates of postprandial lipogenesis in liver and adipose tissue were increased. Thus the changes that were observed in the tumor-bearing animals did not represent a normal response to reduced food intake. Increased postprandial glycogenesis in tumor-bearing rats is likely to be associated with increased gluconeogenesis, thereby increasing energy expenditure. The prolonged high rate of hepatic glycogen synthesis may also delay the initiation of the next meal and thus contribute to the decrease in food intake in cancer cachexia.