Day-old chicks were fed control or manganese (Mn deficient diets ad libitum for 25 d. The chicks subsequently were refed control diet for up to 5 d. Mn deficiency significantly decreased growth rate and feed intake compared to controls. After 25 d of depletion, bone Mn concentration was 2% that of controls and 88% of the deficient chicks exhibited signs of perosis. Sulfate (35SO4) uptake into uronic acid was significantly depressed in cartilage from the Mn-depleted chicks and increased rapidly with refeeding, which may indicate increased glycosaminoglycan (GAG) biosynthesis or increased sulfation of the GAG molecule. In vitro activity of glycosyltransferases suggest that GAG synthesis may be interrupted by Mn deficiency. Somatomedin activity, serum insulin and glucose levels were not influenced significantly by Mn deficiency. Thus, while Mn deficiency decreased growth and GAG synthesis these effects were not mediated by somatomedin.
Weanling male rats were fed control ad libitum, zinc-deficient (ZD, 1 ppm zinc) or pair-fed (PF) control diets for 13 days. Rats subsequently were refed control diets for up to 8 days and serially killed. ZD and PF diets significantly decreased growth rate, feed intake, and feed efficiency compared to controls. Body weight and feed efficiency, but not feed intake, were significantly less in ZD compared to PF. Bone zinc was 315, 286, and 109 micrograms/g (p less than 0.0001) for control, PF, and ZD at the end of depletion. 35SO4 uptake by glycosaminoglycans (GAG) was significantly less in ZD compared to either control ad libitum or PF rats. Xylosyltransferase activity was decreased significantly below PF and control by ZD, suggesting depressed enzyme activity and/or decreased GAG acceptor sites. Bioassayable somatomedin (Sm) activity was 0.81, 0.42 and 0.33 +/- 0.09 relative activity for control, PF and ZD at the end of depletion. Sm was statistically less in ZD compared to PF at day 2 and 5 of refeeding, but not at the end of depletion. Sm activity and GAG metabolism returned to normal after refeeding for 2-5 days in PF and for 5-8 days in ZD rats. Serum insulin but not glucose was significantly depressed by ZD and PF diets. Thus, zinc deficiency depressed growth and cartilage metabolism and was associated with decreased Sm activity and insulin levels. Some of these changes could be attributed to decreased feed intake as a result of ZD.
The effects of lysine-, methionine- or histidine-deficient diets compared to a control diet fed ad libitum or 15, 10 or 5 g/d were studied in weanling rats. Feed intake was 5-7 g/d for the amino acid-deficient animals. After 3 wk, all amino acid-deficient rats had lost more weight (P less than 0.01) than the controls fed at comparable energy levels. Serum somatomedin (Sm) activity was significantly decreased in lysine- (0.55 U/ml), methionine- (0.32 U/ml) and histidine-deficient (0.38 U/ml) rats compared to rats fed the control diet ad libitum (1.6 U/ml). Differences between amino acid-deficient and calorie-restricted animals were not significant. A similar response was observed in 35SO4 uptake by cartilage glycosaminoglycans (GAG). Caloric restriction and amino acid deficiency each resulted in lower 35SO4 uptake by cartilage GAG than occurred with ad libitum feeding, but there were no significant differences between the rats fed amino acid-deficient diets and those fed 5 or 10 g of the control diet. Compared to rats fed the control diet ad libitum, plasma growth hormone (GH) concentrations were lower in the rats fed 5 or 10 g of control diet per day and in those fed amino acid-deficient diets (P less than 0.05), but GH concentrations were not consistent with the growth retardation observed. The results confirm that Sm and GAG activities are reduced in protein-energy restriction independent of GH. However, changes could not be attributed to specific deficiencies of lysine, methionine and/or histidine.
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