The objectives of this study were to determine whether dietary manganese deficiency alters total glycosaminoglycan (GAG) concentration and composition and glycosyltransferase activity in rat aortas. Sprague-Dawley rats were fed either a manganese-deficient or a manganese-sufficient diet. Arterial GAGs were isolated and quantified by measuring uronic acid content. The individual GAGs were separated and quantified with cellulose acetate electrophoresis. The activity of the enzyme galactosyltransferase I was measured using a 100,000 g particulate fraction and 4-methylumbelliferylxyloside (Xyl-MU) as an acceptor. There was a significant decrease (p < or = 0.05) in uronic acid content in the manganese-deficient (1.18 +/- 0.08 mg/g) rat aortas as compared with the manganese-sufficient (1.59 +/- 0.10 mg/g) ones. Chondroitin sulfate and heparan sulfate concentrations were decreased by 38% (p < or = 0.01) and 36% (p < or = 0.05), respectively, in the manganese-deficient rat aortas. The incorporation of UDP-galactose to acceptors by the manganese-deficient rat aorta preparations was increased by 28% as compared to the manganese-sufficient preparations. These results indicate that manganese is involved in arterial GAG metabolism by affecting the enzyme galactosyltransferase and that changes in GAG concentration and composition with manganese deficiency may ultimately affect arterial wall integrity and subsequently cardiovascular health. This is the first work to demonstrate that manganese nutrition is important in arterial GAG metabolism.

Two experiments were conducted to determine the effect of dietary manganese on cholesterol and lipid metabolism in the Wistar rat and the genetically hypercholesterolemic RICO rat. Weanling animals were placed on a manganese-deficient (0.12 microgram/g) and a supplemented diet (100.12 micrograms/g). Mean body weights, hepatic fatty acid synthesis and liver manganese concentration significantly decreased in the deficient group of Wistar rats. Plasma cholesterol, VLDL (very low density lipoprotein) and HDL (high-density lipoprotein) cholesterol, hepatic cholesterol synthesis, liver cholesterol and lipid concentrations were not significantly affected by manganese deficiency. Mean body weights and hepatic manganese content were lower in the manganese-deficient group in both normal and hypercholesterolemic RICO rats. Manganese deficiency significantly decreased LDL cholesterol concentration in the hypercholesterolemic RICO rats. Manganese deficiency had no significant effect on hepatic cholesterol and fatty acid synthesis, plasma cholesterol, VLDL and HDL cholesterol concentrations, liver lipid and liver cholesterol concentration in either group of RICO rats. These results indicate that dietary manganese deficiency does not result in significant alterations in cholesterol and lipid metabolism in the rat.

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Three experiments were conducted to determine the affect of dietary manganese on cholesterol and lipid metabolism in avian species. In the first experiment, day-old chicks were fed a manganese-deficient (4.8 micrograms/g) and a manganese-supplemented (104.8 micrograms/g) diet for 4 weeks after which time they were injected with estrogen (5 mg diethylstilbestrol per kilogram body weight). Manganese deficiency did not significantly alter plasma or liver cholesterol in either group. Estrogen administration significantly increased plasma cholesterol concentration in both dietary groups and liver cholesterol in the manganese-deficient group. In the second experiment, 15-week-old White Leghorn pullets were fed a manganese-deficient (4.5 micrograms/g) diet for 10 weeks. Although dietary manganese deficiency significantly decreased hepatic manganese and cholesterol concentrations, it did not affect hepatic cholesterol and fatty acid synthesis, liver lipid, plasma or egg yolk cholesterol. Similar results were obtained in the third experiment with older (36-week-old) laying hens given similar manganese-deficient and adequate diets. These results indicate that dietary manganese deficiency in the avian species does not result in a significant alteration of cholesterol and lipid metabolism.