Byrne M M, Pluntke K, Wank U, Schirra J, Arnold R, Göke B, Katschinski M
Department of Gastroenterology and Endocrinology, University of Marburg, Germany.
Eur J Clin Invest. 1998 Jan;28(1):72-8. doi: 10.1046/j.1365-2362.1998.00240.x.
Acute hyperglycaemia is known to inhibit jejunal interdigestive motility. This study was undertaken to establish the effects of hyperglycaemia on fed jejunal motility and small intestinal transit time, and to establish if the effects of hyperglycaemia are mediated in part by hyperinsulinaemia.
Nine healthy male volunteers were studied in random order using three experimental conditions: (a) euglycaemic clamp [glucose 5 mmol L(-1)]; (b) hyperglycaemic clamp [glucose 15 mmol L(-1)]; and (c) euglycaemic hyperinsulinaemic clamp [glucose 5 mmol L(-l)]. Fed jejunal motility was induced by an intrajejunal perfusion of lipid (Lipofundin medium-chained triglyceride 10%) at 1.5 mL min(-1) [1.5 kcal min(-1)] for 180 min through the most proximal port of a manometry catheter (eight ports spaced at 2-cm intervals) located just distal to the ligament of Treitz. One minute after starting the lipid perfusion, 15 g of lactulose dissolved in 20 mL of tap water was infused. Small intestinal transit time was measured by the hydrogen breath test.
Acute hyperglycaemia reduced the total number of jejunal contractions and progradely propagated contractions, the motility index (P < 0.05) and the mean amplitude of contractions and delayed intestinal transit time. Hyperinsulinaemia reduced the total number of jejunal contractions, motility index (P < 0.05) and intestinal transit time.
Thus, hyperinsulinaemia may contribute to the inhibitory effects of hyperglycaemia on jejunal motility. In addition, this study demonstrated that intrajejunal infusion of lipid stimulates sustained glucagon-like peptide-1 release. In contrast to fat-induced gastric inhibitory polypeptide release, this glucagon-like peptide-1 release is not inhibited by exogenous or endogenous hyperinsulinaemia (P = 0.59).
已知急性高血糖会抑制空肠消化间期运动。本研究旨在确定高血糖对进食后空肠运动和小肠转运时间的影响，并确定高血糖的影响是否部分由高胰岛素血症介导。
9名健康男性志愿者按随机顺序接受三种实验条件研究：(a) 正常血糖钳夹 [葡萄糖5 mmol/L(-1)]；(b) 高血糖钳夹 [葡萄糖15 mmol/L(-1)]；(c) 正常血糖高胰岛素钳夹 [葡萄糖5 mmol/L(-1)]。通过位于Treitz韧带远端的测压导管（8个端口，间隔2 cm）最近端端口，以1.5 mL/min(-1) [1.5 kcal/min(-1)] 的速度向空肠内灌注脂质（Lipofundin中链甘油三酯10%）180分钟，诱导进食后空肠运动。在开始脂质灌注1分钟后，输注溶解于20 mL自来水中的15 g乳果糖。通过氢呼气试验测量小肠转运时间。
急性高血糖减少了空肠收缩总数和向前传播的收缩、运动指数（P<0.05）以及收缩的平均幅度，并延迟了肠道转运时间。高胰岛素血症减少了空肠收缩总数、运动指数（P<0.05）和肠道转运时间。
因此，高胰岛素血症可能促成高血糖对空肠运动的抑制作用。此外，本研究表明空肠内输注脂质可刺激胰高血糖素样肽-1持续释放。与脂肪诱导的胃抑制性多肽释放不同，这种胰高血糖素样肽-1释放不受外源性或内源性高胰岛素血症抑制（P = 0.59）。
