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Department of Biochemistry, University of Wisconsin, Madison, Wisconsin
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.
2 Present address: Department of Nutritional Research, Mead Johnson Research Center, Evansville, Indiana.
Manuscript received 28 January 1966.
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