Bell R H, McCullough P J, Pour P M
Department of Surgery, Veterans Administration Medical Center, Cincinnati, Ohio 45220.
Am J Surg. 1988 Jan;155(1):159-64. doi: 10.1016/s0002-9610(88)80274-5.
Clinical studies suggest that diabetes mellitus may predispose to the development of pancreatic cancer. The current study investigated the effect of experimental diabetes on the susceptibility of the Syrian hamster to the induction of exocrine pancreatic carcinoma by the carcinogen BOP. Diabetes was induced with the B-cell toxin streptozotocin. Three groups of animals were studied: nondiabetic control animals and animals with streptozotocin-induced diabetes, and a third group of animals in which the diabetogenic effect of streptozotocin was blocked with nicotinamide. Streptozotocin-induced diabetes significantly inhibited the induction of pancreatic carcinoma by BOP, decreasing the incidence of carcinoma to 24 percent compared with an incidence of 75 percent in nondiabetic control animals (p less than 0.002). In diabetic animals, the degree of inhibition of carcinogenesis paralleled the severity of the diabetes. Blocking the diabetogenic effect of streptozotocin with nicotinamide restored the incidence of induced invasive pancreatic carcinoma to that occurring in nondiabetic control animals. In the hamster model, diabetes appears to have a strong influence on susceptibility to the development of pancreatic carcinoma.
临床研究表明，糖尿病可能易引发胰腺癌。本研究调查了实验性糖尿病对叙利亚仓鼠易受致癌物BOP诱导发生外分泌性胰腺癌的影响。采用B细胞毒素链脲佐菌素诱导糖尿病。研究了三组动物：非糖尿病对照动物、链脲佐菌素诱导糖尿病的动物，以及第三组用烟酰胺阻断链脲佐菌素致糖尿病作用的动物。链脲佐菌素诱导的糖尿病显著抑制了BOP诱导的胰腺癌，使癌发生率降至24%，而在非糖尿病对照动物中癌发生率为75%（p<0.002）。在糖尿病动物中，致癌作用的抑制程度与糖尿病的严重程度平行。用烟酰胺阻断链脲佐菌素的致糖尿病作用可使诱导的侵袭性胰腺癌发生率恢复到非糖尿病对照动物的水平。在仓鼠模型中，糖尿病似乎对胰腺癌发生的易感性有很大影响。
