Jin Sang-Man, Choi Seong Ho, Choi Dong-Wook, Heo Jin Seok, Suh Sunghwan, Bae Ji Cheol, Kim Jae Hyeon, Lee Myung-Shik, Kim Kwang-Won, Lee Moon-Kyu
Division of Endocrinology and Metabolism, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-Dong, Gangnam-Gu, Seoul, 135-710, Republic of Korea.
Endocrine. 2014 Nov;47(2):493-9. doi: 10.1007/s12020-013-0159-9. Epub 2014 Jan 23.
Role of impaired suppression of glucagon secretion in the pathogenesis of pancreatic cancer-associated diabetes has been suggested. We examined the correlation between glucagon/insulin ratio (G/I) after glucose challenge and hemoglobin A1C (A1C) in subjects with and without pancreatic cancer. Data were gathered from a preoperative screening 75-g oral glucose tolerance test in patients who would eventually undergo pancreatic resection. A multiple linear regression analysis was conducted using the following covariates: age, body mass index, hemoglobin, glucose and insulin levels at the corresponding time points, indices of insulin resistance, duration of diabetes, insulinogenic index, and use of glucose-lowering drugs. In subject group with pancreatic cancer (n = 45), but not in subject group without pancreatic cancer (n = 101), participants with A1C ≥ 6.5 % had significantly higher glucagon levels, lower insulin levels, and higher G/I ratios after the glucose challenge than those of the subjects with A1C <5.7 %. In the multiple linear regression analysis, there was an independent correlation between post-challenge G/I ratio and A1C in both groups. Some of the patients without pancreatic cancer had inappropriately elevated G/I ratios despite A1C <6.5 %. These patients were characterized by lower insulinogenic indices (p = 0.004) and less insulin resistance (p = 0.008). In conclusion, post-challenge G/I ratio independently correlated with A1C in patients with pancreatic cancer. Although significant, the degree of correlation was weakened in the subjects without pancreatic cancer because some had lower insulin secretory reserve compensated by less insulin resistance, resulting in inappropriately elevated G/I ratios relative to A1C.
胰高血糖素分泌抑制受损在胰腺癌相关糖尿病发病机制中的作用已被提出。我们研究了葡萄糖激发后胰高血糖素/胰岛素比值（G/I）与有无胰腺癌患者糖化血红蛋白（A1C）之间的相关性。数据来自最终接受胰腺切除术患者术前筛查的75克口服葡萄糖耐量试验。使用以下协变量进行多元线性回归分析：年龄、体重指数、血红蛋白、相应时间点的血糖和胰岛素水平、胰岛素抵抗指数、糖尿病病程、胰岛素生成指数以及降糖药物的使用情况。在胰腺癌患者组（n = 45）中，糖化血红蛋白≥6.5%的参与者在葡萄糖激发后胰高血糖素水平显著更高、胰岛素水平更低、G/I比值更高，而在无胰腺癌患者组（n = 101）中则不然。在多元线性回归分析中，两组中激发后G/I比值与A1C之间均存在独立相关性。一些无胰腺癌的患者尽管糖化血红蛋白<6.5%，但其G/I比值却异常升高。这些患者的特征是胰岛素生成指数较低（p = 0.004）且胰岛素抵抗较轻（p = 0.008）。总之，激发后G/I比值与胰腺癌患者的A1C独立相关。虽然有显著相关性，但在无胰腺癌的受试者中相关性程度减弱，因为一些受试者胰岛素分泌储备较低，但通过较轻的胰岛素抵抗得到补偿，导致相对于糖化血红蛋白而言G/I比值异常升高。
