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Alteration in immunoexpression of glucose transporter 2 in liver of tumour‐bearing rats
Author(s) -
DOI CHIHARU,
NOGUCHI YOSHIKAZU,
ITO TAKAAKI,
YOSHIKAWA TAKAKI,
MAKINO TATSUO,
MATSUMOTO AKIHIKO
Publication year - 1998
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1046/j.1365-2613.1998.00035.x
Subject(s) - glucose transporter , glycogen , hexokinase , medicine , endocrinology , biology , staining , transporter , immunohistochemistry , glucose 6 phosphatase , glycolysis , metabolism , enzyme , insulin , biochemistry , genetics , gene
To elucidate interactions between the glucose transport system and hepatic glucose production in the tumour‐bearing state, glycogen storage, expression of glucose transporter isoform 2 (Glut 2) and activities of glucose‐6‐phosphatase (G‐6‐Pase) and hexokinase were histochemically examined in hepatocytes of tumour‐bearing rats. Five male F344 rats, subcutaneously inoculated with methylcholanthrene(MCA)‐induced sarcoma cells were compared with five pair‐fed animals and four ad libitum fed controls. Glycogen storage was markedly decreased in liver cells of tumour‐bearing rats compared to in those of control animals. Glut 2 immunoreactivity was uniformly seen in the cellular membrane of hepatocytes from control animals. In rats bearing sarcoma, the staining intensity was significantly decreased, suggesting that Glut 2 with its bi‐directional transport capacity was down‐regulated in the tumour‐bearing state. Positive staining for hexokinase activity was located in the perivenous area in livers from control animals and was more diffusely located and more intense in livers from tumour‐bearing animals. G‐6‐Pase activity, limited to the peripheral area in livers from controls, extended to the intermediate area and had stronger reactivity in livers from tumour‐bearing animals. In the tumour‐bearing cachectic condition, glucose may be partially consumed by a futile cycle, hepatic metabolic zonation was disturbed, and the release of glucose from the liver may not be mediated by a facilitative glucose transporter‐2.