Green G M, Guan D, Schwartz J G, Phillips W T
Department of Physiology, University of Texas Health Science Center at San Antonio 78284-7756, USA.
Diabetologia. 1997 Feb;40(2):136-42. doi: 10.1007/s001250050654.
Patients with early non-insulin-dependent diabetes mellitus (NIDDM) empty glucose solutions from their stomachs more rapidly than non-diabetic control subjects, and this exacerbates postprandial hyperglycaemia. To determine if accelerated gastric emptying occurred in a rat model of NIDDM and influenced postprandial hyperglycaemia, gastric emptying of glucose was measured, and the effect of slowing the gastric emptying rate on postprandial hyperglycaemia was observed. We tested eight male obese Zucker diabetic rats and eight age-matched lean Zucker controls at 10-13 weeks of age to measure gastric emptying of glucose (by gamma scintigraphy). Rats fasted overnight were gavaged with 30% glucose at 1 ml/100 g body weight. Separately, six Zucker diabetic rats and six lean controls were tested for sensitivity to the inhibitory effects of cholecystokinin and secretin on gastric emptying. The diabetic rats emptied glucose significantly faster than controls (t1/2 = 37.3 +/- 1.5 vs 58.8 +/- 2.3 min in controls), and aging exaggerated this differential. Camostat, a stimulant of cholecystokinin and secretin release, added to the glucose meal significantly slowed gastric emptying (t1/2 = 123 +/- 23 and 166 +/- 19 min, diabetic vs lean, respectively), and significantly reduced postprandial hyperglycaemia in diabetic rats. Compared to Zucker lean controls, Zucker diabetic rats were as sensitive (cholecystokinin) or more sensitive (secretin) to gastrointestinal hormones that inhibit gastric emptying. The results demonstrate accelerated gastric emptying in a rat model of NIDDM, consistant with similar observations in humans with early NIDDM. These results also support the proposal that interventions to slow gastric emptying improve glucose control in this disease.
早期非胰岛素依赖型糖尿病（NIDDM）患者胃内葡萄糖溶液排空速度比非糖尿病对照受试者更快，这会加剧餐后高血糖。为了确定NIDDM大鼠模型中是否发生胃排空加速并影响餐后高血糖，测量了葡萄糖的胃排空情况，并观察了减缓胃排空速度对餐后高血糖的影响。我们对8只10 - 13周龄的雄性肥胖Zucker糖尿病大鼠和8只年龄匹配的瘦Zucker对照大鼠进行测试，以测量葡萄糖的胃排空（通过γ闪烁扫描法）。过夜禁食的大鼠以1 ml/100 g体重的剂量灌胃30%葡萄糖。另外，对6只Zucker糖尿病大鼠和6只瘦对照大鼠进行了胆囊收缩素和促胰液素对胃排空抑制作用的敏感性测试。糖尿病大鼠的葡萄糖排空明显快于对照大鼠（t1/2 = 37.3 ± 1.5分钟，对照大鼠为58.8 ± 2.3分钟），且衰老加剧了这种差异。添加到葡萄糖餐中的卡莫司他（一种胆囊收缩素和促胰液素释放的刺激剂）显著减缓了胃排空（t1/2分别为糖尿病大鼠123 ± 23分钟和瘦大鼠166 ± 19分钟），并显著降低了糖尿病大鼠的餐后高血糖。与Zucker瘦对照大鼠相比，Zucker糖尿病大鼠对抑制胃排空的胃肠激素同样敏感（胆囊收缩素）或更敏感（促胰液素）。结果表明NIDDM大鼠模型中胃排空加速，这与早期NIDDM患者的类似观察结果一致。这些结果还支持了这样的提议，即减缓胃排空的干预措施可改善该疾病的血糖控制。
