Oxidation of 14C-labeled Carbohydrate, Fat and Amino Acid Substrates by Zinc-deficient Rats

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Abstract
To assess the nature of the major metabolic defects resulting from zinc deficiency, the extent and pattern of oxidation to respiratory CO2 of various 14C-labeled substrates were studied in fasted zinc-deficient rats and fasted control rats. Oxidations of intraperitoneally injected tracer doses of 14C-labeled glucose, acetate, palmitate and glutamate were essentially unaffected by zinc deficiency. Oxidation of large doses of glucose and acetate administered on a body surface area (weight2/3) basis also were little affected by zinc deficiency. Energy metabolism appears not to be impaired in the zinc-deficient rat. Oxidation of tracer doses of 14C-labeled leucine and lysine was significantly enhanced in zinc deficiency and, as shown for leucine, this increase was prevented by feeding a zinc-supplemented diet for 31 hours before the 17-hour fast. Also, oxidation of large doses of glutamate, leucine and lysine was enhanced in zinc-deficient rats, but it was shown with the large dose of lysine that about half of the increased oxidation was due to the difference in body weight. However, a portion of the increased oxidation of the large doses of lysine, and presumably of leucine, was due to zinc deficiency per se. These results suggest a defect in protein synthesis in the zinc-deficient rat.