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This Article Full Text Full Text (PDF) All Versions of this Article: 292/1/E324    most recent 00059.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Knop, F. K. Articles by Krarup, T. Search for Related Content PubMed PubMed Citation Articles by Knop, F. K. Articles by Krarup, T.

Increased postprandial responses of GLP-1 and GIP in patients with chronic pancreatitis and steatorrhea following pancreatic enzyme substitution

¹Department of Internal Medicine F, Gentofte Hospital, University of Copenhagen, Hellerup; ²Department of Internal Medicine M, Glostrup Hospital, University of Copenhagen, Glostrup; ³Department of Biostatistics, Novo Nordisk, Bagsværd; ⁴Department of Endocrinology, Hvidovre Hospital, University of Copenhagen, Hvidovre; and ⁵Department of Medical Physiology, The Panum Institute, University of Copenhagen, Copenhagen, Denmark

Submitted 6 February 2006 ; accepted in final form 30 August 2006

We aimed to investigate how assimilation of nutrients affects the postprandial responses of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) and to evaluate the effect of pancreatic enzyme substitution (PES) on insulin secretion in patients with chronic pancreatitis (CP) and pancreatic exocrine insufficiency (PEI). Eight male patients with CP and PEI were studied. Blood was sampled frequently on two separate days after ingestion of a liquid meal with and without PES, respectively. Eight healthy male subjects served as a control group. -Cell responsiveness was estimated as changes in insulin secretion rates in response to changes in postprandial plasma glucose (PG). There was no difference in the PG incremental area under curve (AUC) for patients with and without PES [406 ± 100 vs. 425 ± 80 mM·4 h (mean ± SE), P = 0.8]. The response of total GLP-1 was higher after PES (AUC: 7.8 ± 1.2 vs. 5.3 ± 0.6 nM·4 h, P = 0.01), as was the response of total GIP (AUC: 32.7 ± 7.5 vs. 21.1 ± 8.3 nM·4 h, P = 0.01). Concurrently, both plasma insulin, plasma C-peptide, and total insulin secretion increased after PES (AUC: 17.7 ± 4.2 vs. 13.6 ± 2.9 nM·4 h, P = 0.02; 237 ± 31.4 vs. 200 ± 27.4 nM·4 h, P = 0.005; and 595 ± 82 vs. 497 ± 80 pmol·kg^–1·4 h, P = 0.01, respectively). -Cell responsiveness to glucose was not significantly different on the two study days for patients with CP. These results suggest that the secretion of GLP-1 and GIP is under influence of the digestion and absorption of nutrients in the small intestine and that PES increases insulin secretion.

pancreatic exocrine insufficiency; glucagon-like peptide-1; glucose-dependent insulinotropic polypeptide