Cypryk Katarzyna, Vilsbøll Tina, Nadel Iwona, Smyczyńska Joanna, Holst Jens Juul, Lewiński Andrzej
Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, Polish Mother's Memorial Hospital Research Institute, Lodz, Poland.
Gynecol Endocrinol. 2007 Jan;23(1):58-62. doi: 10.1080/09513590601137004.
Gestational diabetes mellitus (GDM) and type 2 diabetes mellitus (DM2) are suggested to be caused by the same metabolic disorder. Defects in gut hormone-dependent regulation of beta-cell function (entero-insular axis) have been proposed to contribute to the pathogenesis of DM2. The aim of study was to evaluate whether an impaired secretion of glucagon-like peptide-1 (GLP-1) and/or glucose-dependent insulinotropic polypeptide (GIP) could play a role in the development of carbohydrate disorders during pregnancy.
The study group (GDM) consisted of 13 gestational women with diabetes mellitus in whom GDM was diagnosed according to the World Health Organization criteria (75-g oral glucose tolerance test (OGTT)). The control group consisted of 13 pregnant women with normal glucose tolerance (NGT), matched according to age and duration of pregnancy. For all patients, plasma glucose, insulin, GLP-1 and GIP concentrations were evaluated after an OGTT, i.e. at 0, 30, 60, 90 and 120 min after glucose load.
Fasting plasma glucose concentrations were similar in both groups, but the 0-120 min area under the curve (AUC) for glucose was significantly greater in the GDM group than in the NGT group (p < 0.0005). Fasting insulin concentration was higher (p < 0.05) and the 2-h insulin response (AUCtotal) was significantly greater (p = 0.01) in the GDM group than in the NGT group. Insulin resistance was significantly higher in GDM compared with control women (homeostasis model assessment, p = 0.003). Fasting GLP-1 concentrations were higher in the GDM group (p = 0.05), but no differences were observed in GLP-1 response (AUC) between the studied groups. Fasting and stimulated GIP response did not differ between groups at any time of the study (p > 0.05). Positive correlations were observed between fasting GLP-1 and insulin concentration (r = 0.56, p < 0.004) and between fasting GLP-1 and insulin resistance (r = 0.43, p < 0.029).
An impaired secretion of GLP-1 and GIP does not seem to play a major role in the pathogenesis of GDM.
妊娠糖尿病（GDM）和2型糖尿病（DM2）被认为是由相同的代谢紊乱引起的。肠道激素依赖性β细胞功能调节（肠-胰岛轴）缺陷被认为与DM2的发病机制有关。本研究的目的是评估胰高血糖素样肽-1（GLP-1）和/或葡萄糖依赖性促胰岛素多肽（GIP）分泌受损是否在孕期碳水化合物代谢紊乱的发生中起作用。
研究组（GDM）由13例妊娠糖尿病妇女组成，根据世界卫生组织标准（75g口服葡萄糖耐量试验（OGTT））诊断为GDM。对照组由13例糖耐量正常（NGT）的孕妇组成，根据年龄和孕周进行匹配。对所有患者，在OGTT后，即葡萄糖负荷后0、30、60、90和120分钟评估血浆葡萄糖、胰岛素、GLP-1和GIP浓度。
两组空腹血浆葡萄糖浓度相似，但GDM组葡萄糖0-120分钟曲线下面积（AUC）显著大于NGT组（p<0.0005）。GDM组空腹胰岛素浓度较高（p<0.05），2小时胰岛素反应（AUCtotal）显著大于NGT组（p=0.01）。与对照组妇女相比，GDM患者的胰岛素抵抗显著更高（稳态模型评估，p=0.003）。GDM组空腹GLP-1浓度较高（p=0.05），但研究组之间GLP-1反应（AUC）未观察到差异。在研究的任何时间，两组之间空腹和刺激后的GIP反应均无差异（p>0.05）。空腹GLP-1与胰岛素浓度之间（r=0.56，p<0.004）以及空腹GLP-1与胰岛素抵抗之间（r=0.43，p<0.029）观察到正相关。
GLP-1和GIP分泌受损似乎在GDM发病机制中不起主要作用。
