Walvoort H C, Dormans J A, van den Ingh T S
J Inherit Metab Dis. 1985;8(1):38-46. doi: 10.1007/BF01805484.
The pathology of canine glycogen storage disease type II (acid alpha-glucosidase deficiency, GSD II) was studied in three genetically related Lapland dogs and compared to the pathology of human GSD II (McKusick 23230). Canine GSD II closely parallels the infantile form of the human disease, except for the presence of oesophageal dilatation. Generalized glycogen storage particularly affected muscular tissues (skeletal, oesophageal, cardiac and smooth muscle). The altered cells showed glycogen accumulation in the cytosol and in autophagic membrane-bound vacuoles (glycogenosomes). They also showed increased acid phosphatase activity consistent with the lysosomal nature of this storage disorder. The cytopathology in canine and human GSD II appears to evolve from segregation of glycogen during regular cellular autophagy, phagolysosomal accumulation of the undigested glycogen, and eventually rupture of distended glycogenosomes. This study indicates that the usefulness of canine GSD II as an animal model of human disease, extends to the area of pathogenesis.
对三只具有遗传关系的拉普兰德犬的II型犬糖原贮积病(酸性α-葡萄糖苷酶缺乏症,GSD II)的病理学进行了研究,并与人类GSD II(麦库西克23230)的病理学进行了比较。犬GSD II与人类疾病的婴儿型密切相似,但存在食管扩张。全身性糖原贮积尤其影响肌肉组织(骨骼肌、食管肌、心肌和平滑肌)。发生改变的细胞在胞质溶胶和自噬膜结合空泡(糖原小体)中显示糖原积累。它们还显示酸性磷酸酶活性增加,这与这种贮积病的溶酶体性质一致。犬和人类GSD II的细胞病理学似乎是从正常细胞自噬过程中糖原的分离、未消化糖原的吞噬溶酶体积累以及最终扩张的糖原小体破裂演变而来的。这项研究表明,犬GSD II作为人类疾病动物模型的用途扩展到了发病机制领域。