Permert J, Larsson J, Fruin A B, Tatemoto K, Herrington M K, von Schenck H, Adrian T E
Department of Biomedical Sciences, Creighton University School of Medicine, Omaha, Nebraska, USA.
Pancreas. 1997 Jul;15(1):60-8. doi: 10.1097/00006676-199707000-00009.
The diabetes or impaired glucose tolerance that occurs in most patients with pancreatic cancer is characterized by profound insulin resistance. Recent evidence suggests that the diabetes may result from the presence of the tumor rather than being a predisposing factor to development of the malignancy. Some islet hormones have been shown to exhibit diabetogenic effects. To investigate the potential role of these hormones in the diabetic state associated with pancreatic cancer, we measured islet hormones during fasting in pancreatic cancer patients (n = 30), patients with other malignancies (n = 43), and healthy controls (n = 25). Preoperative pancreatic cancer patients were classified as normal glucose tolerance (NGTT), impaired glucose tolerance (IGTT), non-insulin-requiring diabetes (NIRD), and insulin-requiring diabetes (IRD). Nine pancreatic cancer patients were studied after tumor removal by subtotal pancreatectomy. Some preoperative pancreatic cancer patients (n = 19), postoperative patients (n = 9), and controls (n = 8) were also studied during hyperglycemia and following glucagon injection. Fasting plasma C-peptide was elevated in NIRD pancreatic cancer patients compared to controls. Fasting levels of islet amyloid polypeptide (IAPP), glucagon, and somatostatin were elevated in NIRD and IRD patients. IAPP and glucagon, but not somatostatin, normalized following subtotal pancreatectomy. During hyperglycemia, increases in C-peptide and IAPP were seen only in controls and in NGTT and postoperative pancreatic cancer patients. After glucagon infusion, IAPP levels increased in controls and nondiabetic cancer patients; C-peptide levels increased in controls, nondiabetic patients, and NIRD. Responses of C-peptide and IAPP to glucagon normalized after pancreatectomy. During hyperglycemia, glucagon levels fell in all groups except IGTT patients and a decrease in somatostatin concentrations was seen in controls.
大多数胰腺癌患者出现的糖尿病或糖耐量受损的特征是严重的胰岛素抵抗。最近的证据表明，糖尿病可能是由肿瘤的存在引起的，而不是恶性肿瘤发生的 predisposing 因素。一些胰岛激素已被证明具有致糖尿病作用。为了研究这些激素在与胰腺癌相关的糖尿病状态中的潜在作用，我们在空腹状态下测量了胰腺癌患者（n = 30）、其他恶性肿瘤患者（n = 43）和健康对照者（n = 25）的胰岛激素。术前胰腺癌患者被分为糖耐量正常（NGTT）、糖耐量受损（IGTT）、非胰岛素依赖型糖尿病（NIRD）和胰岛素依赖型糖尿病（IRD）。9 例胰腺癌患者在接受胰体尾切除术后进行了研究。一些术前胰腺癌患者（n = 19）、术后患者（n = 9）和对照者（n = 8）也在高血糖期间和注射胰高血糖素后进行了研究。与对照组相比，NIRD 胰腺癌患者的空腹血浆 C 肽升高。NIRD 和 IRD 患者的空腹胰岛淀粉样多肽（IAPP）、胰高血糖素和生长抑素水平升高。胰体尾切除术后，IAPP 和胰高血糖素（而非生长抑素）恢复正常。在高血糖期间，仅在对照组以及 NGTT 和术后胰腺癌患者中观察到 C 肽和 IAPP 增加。注射胰高血糖素后，对照组和非糖尿病癌症患者的 IAPP 水平升高；对照组、非糖尿病患者和 NIRD 患者的 C 肽水平升高。胰切除术后，C 肽和 IAPP 对胰高血糖素的反应恢复正常。在高血糖期间，除 IGTT 患者外，所有组的胰高血糖素水平均下降，对照组的生长抑素浓度降低。 （注：predisposing 一词在医学语境中较难准确翻译，这里保留英文供参考，可根据具体医学知识调整更准确的中文表述）
