Iwasaki M
Nihon Naibunpi Gakkai Zasshi. 1982 Mar 20;58(3):248-58. doi: 10.1507/endocrine1927.58.3_248.
Recently, major resection of the pancreas has been carrier out not only to treat pancreatic carcinoma but also for benign pancreatic diseases. Dragstedt reported that the amount of insulin required to control glycosuria after partial pancreatectomy is much greater than that needed after total pancreatectomy. Although it is thought that diabetes after partial pancreatectomy is considerably different from that after total pancreatectomy, these pathophysiological changes have not been investigated in detail. In the present experiment, changes in carbohydrate and insulin metabolism and glucagon secretion were studied in dogs in order to elucidate the pathophysiology in diabetes after major resection of the pancreas. Immediately after resection of 90% or more of the entire pancreas, diabetes occurred with absolute insulin deficiency, being accompanied by decreased function of the anti-insulin system with poor secretion of glucagon and delayed recovery of blood sugar after the insulin load. Moreover, the half-life of insulin in this group was much longer than that in normal dogs and close to that after total pancreatectomy. These results could explain that the dosage of insulin required to control blood sugar after resection of 90% or more of the entire pancreas was close to that after total pancreatectomy. Six weeks or more after resection of 70 to 90% of the entire pancreas, so-called Sandmeyer's diabetes gradually as a consequence of a decrease in insulin secretion and an increase in glucagon secretion from the remnant pancreas. After the insulin load, glucagon secretion markedly increased and recovery of blood sugar from the insulin hypoglycemia was good, showing hyperfunction of the anti-insulin system. Moreover, the half-life of insulin gradually lengthened but was still shorter than that after total pancreatectomy. These results could well explain the fact that the insulin dosage required to control blood sugar in Sandmeyer's diabetes was 3 to 4 times more than that needed after total pancreatectomy. After resection of less than 70% of the entire pancreas, diabetes did not occur throughout a period of post-operative observation of up to 66 weeks. After the insulin load, glucagon secretion and recovery rate of blood sugar from the insulin hypoglycemia were maintained well, showing normal function of the anti-insulin system, and the half-life of insulin was also within the normal range.
最近,胰腺的大部切除术不仅用于治疗胰腺癌,也用于治疗胰腺良性疾病。德拉格施泰特报告称,部分胰腺切除术后控制糖尿所需的胰岛素量远大于全胰腺切除术后所需的量。虽然人们认为部分胰腺切除术后的糖尿病与全胰腺切除术后的糖尿病有很大不同,但这些病理生理变化尚未得到详细研究。在本实验中,对犬的碳水化合物和胰岛素代谢以及胰高血糖素分泌变化进行了研究,以阐明胰腺大部切除术后糖尿病的病理生理学。在切除整个胰腺的90%或更多后,立即出现了伴有绝对胰岛素缺乏的糖尿病,同时抗胰岛素系统功能下降,胰高血糖素分泌减少,胰岛素负荷后血糖恢复延迟。此外,该组胰岛素的半衰期比正常犬长得多,且接近全胰腺切除术后的半衰期。这些结果可以解释为什么切除整个胰腺的90%或更多后控制血糖所需的胰岛素剂量接近全胰腺切除术后的剂量。在切除整个胰腺的70%至90%后六周或更长时间,由于残余胰腺胰岛素分泌减少和胰高血糖素分泌增加,逐渐出现所谓的桑德迈尔糖尿病。胰岛素负荷后,胰高血糖素分泌明显增加,胰岛素低血糖后血糖恢复良好,显示抗胰岛素系统功能亢进。此外,胰岛素的半衰期逐渐延长,但仍短于全胰腺切除术后的半衰期。这些结果可以很好地解释这样一个事实,即控制桑德迈尔糖尿病血糖所需的胰岛素剂量比全胰腺切除术后所需的剂量多3至4倍。在切除整个胰腺不到70%后,在长达66周的术后观察期内未发生糖尿病。胰岛素负荷后,胰高血糖素分泌和胰岛素低血糖后血糖恢复率保持良好,显示抗胰岛素系统功能正常,胰岛素半衰期也在正常范围内。