REDUCED INCRETIN EFFECT IN TYPE-2 (NON-INSULIN-DEPENDENT) DIABETES
REDUCED INCRETIN EFFECT IN TYPE-2 (NON-INSULIN-DEPENDENT) DIABETES
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DOI：
10.1007/bf02427280
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发表时间：
1986-01-01
期刊：
影响因子：
8.2
通讯作者：
CREUTZFELDT, W
中科院分区：
文献类型：
--
作者：
NAUCK, M;STOCKMANN, F;CREUTZFELDT, W
对14例非胰岛素依赖型2型糖尿病患者和8例年龄和体重相匹配的代谢健康受试者分别测定了口服50g葡萄糖负荷和静脉输注等血糖时的积分递增免疫反应性胰岛素和连接肽反应。口服和静脉注射葡萄糖的反应差异归因于葡萄糖本身以外的其他因素(胰岛素效应)。尽管血糖升高较多，但糖尿病患者口服葡萄糖后的免疫反应胰岛素和连接肽反应延迟。两组的综合反应没有显著差异。然而，在“等血糖”静脉输注期间，由于较高的血糖刺激，糖尿病患者的胰岛素和连接肽反应比对照组更大。胰岛素因子对总胰岛素应答的贡献率为72.8±-。对照组为6.9%(100%=口服负荷反应)和36.0.+-。糖尿病患者中8.8%(p<0.01)。0.05)。对连接肽反应的贡献率为58.4.+-。对照组为7.6%，7.6.+-。14.5%(p.ltoreq.0.05)在糖尿病患者中。胰岛素积分与连接多肽反应的比率表明，与静脉注射葡萄糖相比，对照组口服后(肝脏)胰岛素的摄取量减少。但糖尿病患者的情况并非如此。正常对照组和糖尿病患者的胃抑制多肽反应无明显差异。在2型糖尿病患者中，面对正常的胃抑制性多肽反应，胰岛素效应的减弱或消失可能是由于B细胞对胃抑制性多肽的胰岛素分泌作用的敏感性降低，或对分泌减少或尚未确定的具有胰岛素活性的体液或神经肠道因子的有效性降低所致。
Integrated incremental immunoreactive insulin and connecting peptide responses to an oral glucose load of 50 g and an "isoglycaemic" intravenous glucose infusion, respectively, were measured in 14 Type 2 (non-insulin-dependent) diabetic patients and 8 age- and weight-matched metabolically healthy control subjects. Differences between responses to oral and intravenous glucose administration are attributed to factors other than glucose itself (incretin effect). Despite higher glucose increases, immunoreactive insulin and connecting peptide responses after oral glucose were delayed in diabetic patients. Integrated responses were not significantly different between both groups. However, during "isoglycaemic" intravenous infusion, insulin and connecting peptide responses were greater in diabetic patients than in control subjects as a consequence of the higher glycaemic stimulus. The contribution of incretin factors to total insulin responses was 72.8 .+-. 6.9% (100% = response to oral load) in control subjects and 36.0 .+-. 8.8% in diabetic patients (p .ltoreq. 0.05). The contribution to connecting peptide responses was 58.4 .+-. 7.6% in control subjects and 7.6 .+-. 14.5% (p .ltoreq. 0.05) in diabetic patients. Ratios of integrated insulin to connecting peptide responses suggest a reduced (hepatic) insulin extraction in control subjects after oral as compared to intravenous glucose. This was not the case in diabetic patients. Immunoreactive gastric inhibitory polypeptide responses were not different between control subjects and diabetic patients. A reduced or lost incretin effect in the face of normal gastric inhibitory polypeptide response in Type 2 diabetic patients may be explained by decreased sensitivity of the B cells towards the insulinotropic effect of gastric inhibitory polypeptide or to hyposecretion or reduced effectiveness of as yet unidentified humoral or nervous gut factors with incretin activity.