Abstract
This study was performed to investigate the mechanism involved in a decrease in the serum glucose of golden hamsters infected with plerocercoids of Spirometra erinacei. The concentration of glucagon, the activity of glucose-6-phosphatase in the liver, and the in vivo incorporation of 2-deoxy-D-[1,2-3H]glucose into various organs increased in plerocercoid-infected hamsters compared with controls. Furthermore, the serum from the plerocercoid-infected hamsters enhanced the in vitro incorporation of [U-14C]glucose into adipose tissues, compared with control serum. The serum levels of immunoreactive insulin and somatomedin associated with nonsuppressible insulin-like activity in experimental animals, however, were not significantly different from those in controls. Therefore, we conclude that the decrease in serum glucose associated with plerocercoid infection is not the result of a decrease in gluconeogenesis, but the result of an increased utilization of glucose in the peripheral tissues.
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