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Endocrinology, doi:10.1210/endo-103-5-1541
Endocrinology Vol. 103, No. 5 1541-1545
Copyright © 1978 by the Endocrine Society.
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Biochemical Studies on Rats with Insulin-Secreting Islet Cell Tumors Induced by Streptozotocin: With Special Reference to Physiological Response to Oral Glucose Load in the Course of and after Tumor Induction

TSUTOMU KAZUMI, GEN YOSHINO, YASUAKI YOSHIDA, KUNIHIRO DOI, MUNEYOSHI YOSHIDA, SHIGEO KANEKO and SHIGEAKI BABA

The Second Department of Internal Medicine, Kobe University School of Medicine Kobe, Japan

Address reprint requests to Prof. Shigeaki Baba, The Second Department of Internal Medicine, Kobe University School of Medicine, Kusunoki-cho 7-chome, Ikutaku, Kobe, 650 Japan.

Abstract

Pancreatic islet cell tumors were induced in 32 of 49 male Wistar rats (73%) surviving 9 months or longer following treatment with streptozotocin alone, with streptozotocin and nicotinamide, or with streptozotocin and picolinamide. Serial oral glucose tolerance tests in rats treated with streptozotocin and nicotinamide showed that the elevation of blood glucose levels after Oral glucose load was depressed significantly 7 months after treatment. Plasma insulin responses were distinctly elevated 9 months after treatment. Blood glucose levels remained lower and plasma insulin levels rose markedly after a glucose load in tumor-bearing rats as compared to the response of tumor-free rats. These findings suggest that pancreatic islet cell tumors induced by streptozotocin with and without combined treatment are insulin-secreting, and that streptozotocin itself has oncogenic effects on the rat pancreas. Mean insulin concentration in islet cell tumors amounted to 401 U/g wet wt, whereas the concentration was 14 U/g wet wt in the pancreatic tissue from tumor-free rats.

Received May 12, 1977.






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Copyright © 1978 by The Endocrine Society