Vitamin A and Glycosaminoglycan Metabolism in Rats

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Abstract
Rats were fed diets deficient, marginally adequate, adequate or excessive in vitamin A. The levels of the different glycosaminoglycans of the aorta and liver, some of the enzymes concerned with the biosynthesis and degradation of glycosaminoglycans, levels of PAPS, sulfate activating system and sulfotransferase, lipoprotein lipase and lipid levels of tissues were determined in these rats. Hyaluronic acid decreased in both liver and aorta in the vitamin A-deficient group, while it increased in the aorta but decreased in the liver in the vitamin A-excessive group. The sulfated glycosaminoglycans—heparin sulfate, chondroitin sulfate A, chondroitin sulfate B, chondroitin sulfate C and heparin—all decreased in the aorta in vitamin A deficiency, but increased significantly in the rats of the excessive group. Heparin sulfate and heparin decreased in the liver of the deficiency group, and increased in the excessive group, but the other sulfated glycosaminoglycan fractions decreased in both deficient and excessive groups. L-Glutamine:D-fructose-6-phosphate aminotransferase activity decreased in vitamin A deficiency in both liver and aorta, but increased in the excessive group. UDPG dehydrogenase and UDPG pyrophosphorylase activities were not appreciably affected by vitamin A concentration. β-Glucuronidase activity increased in the liver and aorta in both vitamin A deficiency and hypervitaminosis while β-hexosaminidase activity increased in these tissues in the deficient group, but was not affected in the aorta in the excessive group. Hyaluronidase and chondrosulfatase increased in the deficient group in both liver and aorta, increased in the liver, but decreased in the aorta in the excessive group. Free hexosamines and uronic acids of the liver and aorta increased in both deficient and excessive groups. Hepatic PAPS levels decreased in vitamin A deficiency, but were not appreciably affected in the excessive group. The sulfate activating system (ATP sulfurylase and APS kinase) decreased in the deficiency group, but increased in the excessive group. Sulfotransferase activity decreased in the deficient group and increased in the excessive group. Total cholesterol and triglycerides of the liver and aorta and phospholipids of the aorta increased in vitamin A deficiency, but decreased in the excessive group. On the other hand, phospholipids of the liver decreased in vitamin A deficiency and increased in the excessive group. Lipoprotein lipase activity decreased in the liver, aorta and heart in vitamin A deficiency, but increased in the excessive group.

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