Abstract
Summary
Studies on the liver involved with increasing amounts of amyloidosis and control tissues indicate that there is a marked increase in MPS content with severe amyloid infiltration. The increase of MPS was accounted for by increases in heparitin sulfate, chondroitin sulfate B, and somewhat less of chondroitin sulfates A and C. The consistent increase of heparitin sulfate in the liver of the ducks was similar to that observed in amyloidosis in humans and in experimentally induced disease. This remarkable increase of chondroitin sulfate B suggests a link to other vascular diseases and genetic connective tissue defects. The Pekin duck serves as an interesting model to study spontaneously occurring amyloidosis.
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