Frank J W, Saslow S B, Camilleri M, Thomforde G M, Dinneen S, Rizza R A
Gastroenterology Unit, Mayo Clinic, Rochester, Minnesota, USA.
Gastroenterology. 1995 Sep;109(3):755-65. doi: 10.1016/0016-5085(95)90382-8.
BACKGROUND & AIMS: The roles of hyperglycemia in diabetic gastroparesis and gastric delivery in postprandial hyperglycemia of diabetic patients are unclear. The aims of this study were to assess gastric emptying and its relation to postprandial glucose metabolism in patients with asymptomatic non-insulin-dependent diabetes mellitus (NIDDM) and no autonomic neuropathy and to identify motor mechanisms responsible for any accelerated gastric emptying.
Autonomic function, gastric emptying, postprandial glucose metabolism, and hormone levels (glucagon, insulin, cholecystokinin, glucose-dependent insulinotropic polypeptide, neurotensin, and peptide YY) were assessed in healthy volunteers and patients with NIDDM. In a second study, gastric tone and motility were measured in patients with accelerated gastric emptying and in controls.
Gastric emptying of solids did not differ in the two groups, but liquids emptied faster in patients with NIDDM (P < 0.02). The rate of entry of ingested glucose into the systemic circulation was similar, but higher postprandial glucagon and lower insulin concentrations led to greater (P < 0.01) postprandial hepatic glucose release. Levels of other enteropeptides, gastric accommodation, and antral motility were similar, but patients with NIDDM had greater proximal gastric phasic contractions than controls (P < 0.05).
Excessive hepatic glucose release, not rapid entry of ingested glucose, is the primary cause of postprandial hyperglycemia in patients with NIDDM. Accelerated gastric emptying in patients with nonneuropathic NIDDM is associated with increased proximal stomach phasic contractions.
高血糖在糖尿病胃轻瘫中的作用以及糖尿病患者餐后高血糖时胃排空的情况尚不清楚。本研究的目的是评估无症状非胰岛素依赖型糖尿病（NIDDM）且无自主神经病变患者的胃排空及其与餐后葡萄糖代谢的关系，并确定导致胃排空加速的运动机制。
对健康志愿者和NIDDM患者进行自主神经功能、胃排空、餐后葡萄糖代谢及激素水平（胰高血糖素、胰岛素、胆囊收缩素、葡萄糖依赖性促胰岛素多肽、神经降压素和肽YY）的评估。在第二项研究中，对胃排空加速的患者和对照组进行胃张力和运动性的测量。
两组固体食物的胃排空无差异，但NIDDM患者液体排空更快（P<0.02）。摄入葡萄糖进入体循环的速率相似，但餐后胰高血糖素水平较高和胰岛素浓度较低导致餐后肝脏葡萄糖释放量更大（P<0.01）。其他肠肽水平、胃容纳功能和胃窦运动性相似，但NIDDM患者近端胃的相性收缩比对照组更强（P<0.05）。
NIDDM患者餐后高血糖的主要原因是肝脏葡萄糖过度释放，而非摄入葡萄糖的快速进入。非神经病变性NIDDM患者胃排空加速与近端胃相性收缩增加有关。
