Eliasson B, Björnsson E, Urbanavicius V, Andersson H, Fowelin J, Attvall S, Abrahamsson H, Smith U
Lundberg Laboratory for Diabetes Research, Department of Internal Medicine, Göteborg University, Sahlgrenska University Hospital, Gothenburg, Sweden.
Diabetologia. 1995 Jan;38(1):79-85. doi: 10.1007/BF02369356.
Experimental euglycaemic hyperinsulinaemia (insulin levels 46 +/- 4 mU/l) impaired the post-absorptive gastrointestinal motility in healthy individuals; the effect being particularly pronounced in the upper gastrointestinal tract (stomach and proximal duodenum). The postprandial gastric emptying, measured with a standardized 99mTc labelled meal, was also significantly delayed (t50 increased by 38% or 32 min). This was combined with a slower carbohydrate absorption (delay in peak blood glucose level about 40 min). Furthermore, during experimental hyperinsulinaemia higher blood glucose levels were seen at 120 min than at 60 min after food ingestion. This was not seen in any subject in the control study where only 0.9% NaCl was infused. Blood levels of the motility-stimulating hormone, motilin, were significantly lower during experimental hyperinsulinaemia. Thus, experimental hyperinsulinaemia impairs the gastrointestinal motility in both the postabsorptive and postprandial states. This effect is combined with a delayed carbohydrate absorption. Hyperinsulinaemia per se may thus lead to alterations in carbohydrate absorption and can also contribute to the gastrointestinal disturbances in diabetes.
实验性正常血糖高胰岛素血症（胰岛素水平为46±4 mU/l）损害了健康个体吸收后的胃肠动力；这种影响在上消化道（胃和十二指肠近端）尤为明显。用标准化的99mTc标记餐测量的餐后胃排空也显著延迟（t50增加38%或32分钟）。这与碳水化合物吸收减慢（血糖峰值水平延迟约40分钟）相关。此外，在实验性高胰岛素血症期间，进食后120分钟的血糖水平高于60分钟时。在仅输注0.9%氯化钠的对照研究中，任何受试者均未出现这种情况。在实验性高胰岛素血症期间，刺激动力的激素胃动素的血药浓度显著降低。因此，实验性高胰岛素血症损害了吸收后和餐后状态下的胃肠动力。这种影响与碳水化合物吸收延迟相关。因此，高胰岛素血症本身可能导致碳水化合物吸收改变，也可能导致糖尿病患者的胃肠道紊乱。
