非酒精性脂肪肝患者口服葡萄糖后血浆胰高血糖素样肽和葡萄糖依赖性促胰岛素多肽水平的变化

Changes of GLP-1 and GIP in Patients with Non-alcoholic Fatty Liver Disease after Oral Glucose

目的考察非酒精性脂肪肝(nonalcoholic fatty liver,NAFLD)患者口服葡萄糖后胰高血糖素样肽(glucagonlikepeptide-1,GLP-1)和葡萄糖依赖性促胰岛素多肽(glucose-dependent insulinotropic ploypeptide,GIP)分泌的特征。方法选取34例非酒精性脂肪肝和42例健康人群,行口服糖耐量试验后在120 min内测定血GLP-1、GIP、血糖、血胰岛素、胰高血糖素含量进行比较。结果 NAFLD患者经葡萄糖诱导后GLP-1分泌量明显低于正常对照组(P<0.01),而GIP没有明显改变,但是所有患者均存在胰岛素抵抗。与正常对照组相比,NAFLD患者空腹胰岛素水平和葡萄糖诱导后的胰岛素水平均明显升高,血糖降低缓慢,而空腹胰高血糖素水平明显升高。结论 NAFLD患者经葡萄糖诱导分泌GLP-1功能缺陷,GIP分泌无异常。NAFLD患者存在胰岛素抵抗、高胰岛素血症和胰高血糖素血症。

OBJECTIVE To determine the secretion of incretins after oral glucose administration in non-alcoholic liver disease（NAFLD） patients. METHODS Standardized oral glucose tolerance test was performed on patients with NAFLD（n=34） and healthy controls（n=42）. Glucose, insulin, glucagon, glucagon-likepeptide-1（GLP-1） and glucose-dependent insulinotropic ploypeptide（GIP） plasma levels were measured sequentially for 120 minutes after glucose administration. RESULTS Glucose induced GLP-1 secretion was significantly decreased in patients compared with control group（P〈0.01）. In contrast, GIP secretion was unchanged. All patients were insulin resistant. Fasting and glucose- induced insulin secretion was higher in NAFLD compared with control group, while the glucose lowering effect was diminished. Concomitantly, fasting glucagon secretion was significantly elevated in NAFLD. CONCLUSION Glucose-induced GLP-1 secretion is deficient in patients with NAFLD. GIP secretion is contrarily preserved. Insulin resistance, with hyperinsulinemia and hyperglucagonemia, is present in all patients.