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Amine-Induced Pancreatic Exocrine Tumors in Syrian Hamsters by Exogenous Insulin1

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Amine-Induced Pancreatic Exocrine Tumors in Syrian Hamsters by Exogenous Insulin1 (CANCER RESEARCH 50, 1634-1639. March 1. 1990| Inhibition of Streptozotocin-induced Islet Cell Tumors and 7V-Nitrosobis(2-oxopropyl)amine-induced Pancreatic Exocrine Tumors in Syrian Hamsters by Exogenous Insulin1 Parviz M. Pour,2 Katherine Kazakoff, and Kim Carlson The Eppley Institute and Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska 68105-1065 ABSTRACT in hamsters, but animals recover from their diabetes sponta The effects of streptozotocin (SZ) and /V-nitrosobis(2-oxopropyl)amine neously. This recovery was associated with increased cell rep lication in islet and duetti lar cells with a peak 14 days post-SZ (BOP), separately or in combination, on the pancreas, common duct, and treatment.4 Treatment of diabetic hamsters with insulin pre gallbladder, all target tissues of BOP, were studied in Syrian golden hamsters. Groups of hamsters were treated with either a single dose (20 vented spontaneous recovery from diabetes and inhibited the mg/kg body weight) of BOP (BOP group), or a single i.p. dose (§0mg/ SZ-induced increase in cell replication of islet and ductular kg body weight) of SZ and 14 days later with a single s.c. injection of the cells.4 same dose of BOP (SZ + BOP group). Another group of animals was In the present study we examined the effect of SZ alone or treated similarly with BOP and SZ except that they received twice daily in combination with insulin on the induction by BOP of pan injections of insulin, beginning 1 day after SZ administration and for the creatic exocrine tumors, which are morphologically and biolog duration of the experiment (52 weeks) (SZ + insulin + BOP group). The ically similar to the human disease (11, 12). If cell proliferation control group consisted of hamsters treated with a single dose of BOP and daily doses of insulin (insulin + BOP group). Hamsters treated with in diabetic hamsters renders pancreatic cells more vulnerable SZ recovered spontaneously from their diabetes, although the mortality to the carcinogenic action of BOP, more tumors would be was high (86%). BOP treatment inhibited the diabetogenic effects of SZ expected in diabetic than in nondiabetic hamsters. On the other in both SZ + BOP and SZ + insulin + BOP groups and reduced the hand, insulin would counteract the enhancing effect of SZ on mortality to 43 and 74%, respectively. SZ pretreatment inhibited the exocrine pancreatic cancer induction because of its suppressive incidence of BOP-induced pancreatic ductal/ductular cell carcinomas in effects on cell replication. We also examined the common duct the SZ + BOP group (P< 0.01); this protective effect of SZ on carcinoma and the gallbladder, other target tissues of BOP. development was potentiated by additional treatment with insulin (SZ + insulin + BOP group, P < 0.001). Although the frequency of BOP- induced tumors in the gallbladder (all polyps) was not altered by either MATERIALS AND METHODS SZ or insulin, the frequency of the common duct polyps was significantly lower in the SZ + insulin + BOP group than in the BOP group (P < Male Syrian hamsters from the Eppley colony were housed in groups 0.005). Hamsters in the SZ, SZ + BOP, and SZ + insulin + BOP groups of 5 in plastic cages on granular cellulose bedding [Bed-O-Cobs; The developed islet cell adenomas (insulomas). However, the SZ + insulin + Anderson Cob Division, Maumee, OH], kept under standard laboratory BOP group had significant!) fewer insulomas than in the SZ + BOP conditions [room temperature, 21 ±3°C;12-h light/12-h dark cycle; group (/' < 0.0005). The overall data confirm the inhibitory effect of SZ relative humidity, 40 ±5% (SD)], and given Wayne Lab Blox (Allied on BOP-induced pancreatic cancer and suggest that this effect is related Mills, Chicago, IL) and water ad libitum. to the diabetic condition of hamsters rather than insulin deficiency and Hamsters were divided into 5 groups, 50 each, and were treated as that intact islets appear to be prerequisite for exocrine pancreatic cancer follows: BOP alone (BOP group); BOP plus twice daily insulin (see induction by BOP. On the other hand, the inhibitory action of insulin on below) for life (insulin + BOP groups); BOP plus SZ (SZ + BOP insuloma induction by SZ and on ductal/ductular cancer induction by BOP seems to be related to the suppressive effect of this hormone on />'- group); BOP plus SZ plus daily insulin for life (SZ + insulin + BOP group); SZ alone (SZ group; Table 1). The dose of BOP was 20 mg/kg cell and ductal/ductular cell replication, respectively. body weight and that of SZ was 50 mg/kg body weight. All animals were 8 weeks old when the treatment began. Surviving INTRODUCTION hamsters were sacrificed by CO2 inhalation. Blood glucose levels were Epidemiological studies suggest that diabetes presents a pre determined once before the treatment, every 8 weeks thereafter until disposing factor for pancreatic cancer (1-6) and that the risk of 28 weeks, and at the termination of the experiment at 52 weeks. At autopsy, all organs were examined grossly. The pancreas, with pancreatic cancer development remains for years after the di attached gallbladder and common duct, were fixed in Bouin's solution, agnosis of diabetes (1). Moreover, histopathological studies processed for histology by conventional methods, and stained with have revealed hyperplastic changes in the pancreatic ducts of hematoxylin and eosin. From 10 hamsters each from the SZ and SZ + deceased diabetics more often than in those of nondiabetics (7). insulin + BOP groups, the tissues were examined immunohistochemi- Reasons for the particular predisposition of diabetics toward cally for demonstration of ß-,«-,and á-cellsby using the appropriate pancreatic cancer could include perpetual proliferation of duc- antibodies as described.4 tular cells in diabetic patients (8, 9), a condition known to BOP was synthesized as reported ( 13) and was given once s.c. SZ (Sigma Chemical Co., St. Louis, MO), was prepared immediately increase the risk for carcinogenesis in many tissues, including before use as a 10-mg/ml solution in 0.1 M citrate buffer (pH 4.5) and the pancreas (10). was given i.p. as described.4 Our previous study has shown that SZ3 causes severe diabetes Insulin (Eli Lilly and Co., Indianapolis. IN) was prepared in normal Received 5/12/89; revised 8/7/89, 11/13/89; accepted 11/15/89. saline and injected s.c. twice a day during the experiment. Hamsters The costs of publication of this article were defrayed in part by the payment received 4 units Lente and 1 unit regular insulin/kg body weight 2 h of page charges. This article must therefore be hereby marked advertisement in before the dark cycle began (at 4 p.m.) and then received 4 units Lente accordance with 18 U.S.C. Section 1734 solely to indicate this fact. 1Supported by Grant CA38922. Laboratory Core Grant CA36727. National and 4 units Ultra Lente/kg body weight 16 h later (at 8 a.m. the Cancer Institute/NIH. and S1G-16. American Cancer Society. following day). Injection of each insulin type was given by separate 2To whom requests for reprints should be addressed, at The Eppley Institute syringe. This treatment schedule was found to be optimal in controlling for Research in Cancer, University of Nebraska Medical Center, 42nd and Dewey Avenue. Omaha. NE 68105-1065. 4 P. M. Pour. W. Duckworth, K. Carlson, and K. Kazakoff. Insulin therapy ' The abbreviations used are: SZ, streptozotocin; BOP. A'-nitrosobis(2-oxopro- prevents spontaneous recovery from streptozotocin-induced diabetes in Syrian pyl)amine. hamsters, submitted for publication. 1634 Downloaded from cancerres.aacrjournals.org on September 29, 2021. © 1990 American Association for Cancer Research. INSULIN EFFECTS ON SZ AND BOP CARCINOGENESIS Table I Effective number of animals (ENA), survivals and final body weights (bw), type and incidence of tumors induced in Syrian hamsters with BOP and/or SZ with or without insulin treatment Given p values correspond to the data comparison between the groups with the same letters, i.e., a with a. b with h, etc. ductpolypsno. +SD)48 bw(g)130 bw(g)127 (%)Oa1 (%)14(42)°-*14(41)'-''9(21)4(%)1 (%)18(54)°16(47)*19(54)*14(33)'o°-*-r•(%)14(42)°-*13(38)°'*9(32)3 BOPGroupInsulin ±745 11132± 11136±± 1(33)°-*-'7 BOPSZ + 1048± 13124± 32135 (3)"22 (20)"3(7)*1 +SZ ±642 13120± ±21126 (52)0-*-''4(9)''7(21)'° +SZBOPinsulin+BOPENA3334424315Survival(wk±945 10118± 22138± (9)°-'o*-"° (2)°-"Of'c"P< (8)°0*° ±10Initial ±21Final ±17Insulomano. 0.0005*P< 0.005*P< 0.001*/><O.OI' 0.005*/><O.OI'P< 0.005*P< 0.0005'P< 0.025'P< P < 0.025 0.001°><P< 0.005"><P< 0.025"><P< P < 0.05Common 0.0005Adenomano.0.025Carcinomano.0.025Gallbladderpolypsno. hyperglycemia without adverse effects.4 value at week 30. The rate of survival in hamsters from the SZ Determination of Blood Glucose. Under light ether anesthesia blood + BOP group was significantly higher (57%) than in the SZ was withdrawn from the orbital vein and glucose was determined by group. the glucose oxidase method. In hamsters treated with SZ + insulin + BOP, the blood Statistical Analysis. Data were given as mean ±SD. For statistical comparison, analysis of variance by Scheffe's method was used. For glucose levels were high and remained high until week 16, at which time they were higher than levels in SZ-treated hamsters tumor incidence, data were considered from hamsters that lived longer than 28 weeks, at which time the first tumor was detected.
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