Type II diabetic patients with no clinical evidence of neuronal dysfunction have a significantly more rapid rate of gastric emptying of a solid high-carbohydrate meal when compared with nondiabetic control subjects.

A trypsin/chymotrypsin inhibitor, POT II, can delay the rate of gastric emptying, and decrease postprandial plasma glucose levels, GIP levels, and serum insulin levels in type II diabetic patients diagnosed recently. Delay of gastric emptying in diabetic patients may provide a unique or adjunctive approach to the treatment of type II diabetes.

In a previous study we demonstrated that patients with recently diagnosed non-insulin-dependent diabetes mellitus (NIDDM) had significantly increased gastric emptying rates of glucose solutions compared with those of nondiabetic sex- and age-matched controls. This finding of rapid gastric emptying contrasts with the delayed gastric emptying often exhibited as a late manifestation of diabetes mellitus that is attributed to autonomic neuropathy. The purpose of this study was to determine, in seven of the patients previously studied, whether (1) an intravenous infusion of cholecystokinin-8 (CCK-8) would delay the gastric emptying of a liquid glucose meal and, if so, (2) whether the delay in gastric emptying would result in reduced postprandial blood glucose concentrations due to prolongation of the absorption of the glucose in the liquid meal. Each patient underwent two separate gastric emptying studies, one during a saline infusion and one during a CCK-8 infusion. Blood samples were obtained at 15-min intervals for measurement of glucose, insulin, CCK-8, and gastric inhibitory polypeptide (GIP) concentrations. The average gastric half-emptying time was 41 min with the saline infusion and 94 min with the CCK-8 infusion (P = 0.0042). The average glucose concentration over the 2-hr period following glucose ingestion was 17.1 mmol/liter with the saline infusion and 14.0 mmol/liter with the CCK-8 infusion (P = 0.0073). The average glucose excursion value over the 2-hr period was reduced from 5.6 mmol/liter to 3.7 mmol/liter with the CCK-8 infusion (P = 0.0550).(ABSTRACT TRUNCATED AT 250 WORDS)

Phillips et al. [1] demonstrated abnormally rapid gastric emptying of glucose solutions in patients with recently diagnosed non-insulin-dependent diabetes mellitus (NIDDM), which contrasts with delayed gastric emptying (gastroparesis), a well-documented late manifestation of diabetes attributed to autonomic neuropathy [2]. Intravenous administration of cholecystokinin (CCK), a physiological inhibitor of gastric emptying in healthy humans [3], normalized gastric emptying of a glucose test meal in NIDDM diabetic patients and reduced the postprandial hyperglycaemia [4]. This outcome was predicted from studies in healthy human subjects which showed that CCK regulated postprandial blood glucose levels by slowing gastric emptying [5]. These studies support the hypothesis [1] that accelerated gastric emptying in early NIDDM in humans may contribute to poor glucose control by increasing the rate of glucose entry into the small intestine, thereby increasing absorption rate and exacerbating postprandial hyperglycaemia.To further examine this phenomenon, the gastric emptying of glucose was investigated in a newly Diabetologia (1997) Summary 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 (t 1/2 = 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 (t 1/2 = 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 may improve glucose control in this disease. [Diabetologia (1997) 40: 136-142]

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