, Volume 36, Issue 10, pp 1361-1370

Emptying of the gastric substitute, glucagon-like peptide-1 (GLP-1), and reactive hypoglycemia after total gastrectomy

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Postprandial glucagon-like peptide-1 (GLP-1), pancreatic glucagon, and insulin were measured in 27 tumor-free patients 43 months (median) after total gastrectomy and in four controls using a99technetium-labeled 100-g carbohydrate solid test meal. Emptying of the gastric substitute was measured by scintigraphy. Fourteen patients suffered from early dumping symptoms, and five of them also reported symptoms suggestive of reactive hypoglycemia (late dumping). The median emptying half-time (T1/2) of the gastric substitute was 480 sec. Sigstad's dumping score was 8.5±1.6 (mean±se) in patients with rapid emptying (T1/2<480 sec), and 3.0±1.5 in patients with slow emptying of the gastric substitute (P=0.02). The peak postprandial concentration of GLP-1 was 44±20 pmol/liter in controls, 172±50 in patients without reactive hypoglycemia, and 502±116 in patients whose glucose fell below 3.8 mmol/liter during the second postprandial hour. Plasma GLP-1 concentrations peaked at 15 min, and insulin concentrations at 30 min after the end of the meal. A close correlation between integrated GLP-1 responses and integrated insulin responses (r=0.68) was observed. Multiple regression revealed that three factors were significantly associated with the integrated glucose concentrations during the second hour (60–120 min): Early (first 30 min) integrated GLP-1 (inverse correlation;P=0.006), age (P=0.006), and early integrated pancreatic glucagon (P=0.005). There was a close (inverse) relationship ofT1/2 with early integrated GLP-1 and pancreatic glucagon, but not with insulin. Gel filtration of pooled postprandial plasma of gastrectomized individuals revealed that all glucagon-like immunoreactivity eluted atK d 0.30 (K d , coefficient of distribution), the elution position of glicentin. Almost all of the GLP-1 like immunoreactivity eluted atK d 0.60, the elution position of gut GLP-1. The authors contend that GLP-1-induced insulin release and inhibition of pancreatic glucagon both contribute to the reactive hypoglycemia encountered in some patients following gastric surgery. Rapid emptying seems to be one causative factor for the exaggerated GLP-1 release in these subjects.