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We have recently shown that patients with chronic pancreatitis and pancreatic exocrine insufficiency exhibit greater postprandial responses of the intestinal hormone glucagon-like peptide-2 (GLP-2) as compared to healthy control subjects [1]. GLP-2 is a 33-amino acid peptide hormone secreted by the endocrine L cells of the intestinal mucosa following meal ingestion [2]. It acts as a growth factor in the small intestine [3] and, in patients with functional short-bowel syndrome, GLP-2 has been shown to improve intestinal absorption [4]. Furthermore, GLP-2 seems to increase intestinal blood flow [5], including blood flow in the superior mesenteric artery of pigs [6] and humans [7]. Interestingly, our recent observation of increased postprandial GLP-2 responses in patients with chronic pancreatitis and pancreatic exocrine insufficiency correlated with increased postprandial blood flow in the superior mesenteric arteries of these patients [1]. However, the mechanisms behind the increased postprandial GLP-2 response in chronic pancreatitis patients with pancreatic exocrine insufficiency could only be speculated upon, with one explanation being that reduced assimilation of nutrients in the proximal part of the small intestine results in delivery of a larger nutrient load to the distal L cell-rich part of the small intestine. Reduced assimilation of nutrients in chronic pancreatitis patients with pancreatic exocrine insufficiency can be clinically modulated by the administration of pancreatic enzyme supplementation. In 2007, we reported that pancreatic enzyme supplementation in these patients resulted in increased postprandial secretion of GLP-2’s sister peptide, GLP-1, also released from intestinal L cells [8]. In order to investigate potential mechanisms behind exaggerated GLP-2 levels in chronic pancreatitis we evaluated the impact of pancreatic enzyme supplementation on postprandial GLP-2 responses in the chronic pancreatitis patients from our 2007 study [8]. Eight patients with chronic pancreatitis and pancreatic exocrine insufficiency were investigated using two liquid meal tests consumed with and without two capsules of pancreatic enzyme supplementation (Creon 25,000 U, Solvay Pharma, Herlev, Denmark) as previously described [8]. A group of 8 healthy sexageand body mass index-matched control subjects was examined using the same meal. Arterialized blood was drawn and distributed into EDTA tubes containing aprotinin and a dipeptidyl peptidase 4 (DPP4) inhibitor as previously described [8]. The tubes were centrifuged for 20 minutes at 1,700 g and 4°C, and plasma was stored at -20 °C until analysis. The GLP-2 radioimmunoassay employs antiserum code no. 92160 and standards of human GLP-2 (proglucagon 126-158, a gift from Novo Nordisk A/S, Bagsvaerd, Denmark) and monoiodinated Tyr-12 GLP-1, specific activity greater than 70 MBq/nmol. The antiserum is directed against the N-terminus of GLP-2 and therefore measures only fully processed intact GLP-2 of intestinal origin. Sensitivity for the assay is below 2 pmol/L and the intra-assay coefficient of variation is below 6% [9]. Data are expressed as mean±SEM and were compared by means of analysis of variance (ANOVA). Area under curve (AUC) values were calculated using the trapezoidal rule. Received June 14, 2010 Accepted July 23, 2010

jop : journal of the pancreas

The impact of pancreatic enzyme supplementation on postprandial responses of glucagon-like Peptide-2 in patients with chronic pancreatitis and pancreatic exocrine insufficiency.