Alterations in Digestive Function Caused by Pancreatic Disease

Doty, Jeffrey E.; Fink, Aaron S.; Meyer, James H.

doi:10.1016/s0039-6109(16)44830-9

Cited by 8 publications

(2 citation statements)

References 90 publications

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“…Against this is the observation made by Ebert and Creutzfeldt (12) that PES does not change the GIP response to oral glucose in patients with CP and PEI. Last, we wanted to study the patients with CP as close as possible to their habitual gastrointestinal condition (10). Therefore, the patients were examined with PES during the first experimental day (day 1).…”

Section: Discussionmentioning

confidence: 99%

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

Knop

Vilsbøll²,

Larsen³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

100

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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. beta-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). beta-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.

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Section: Discussionmentioning

confidence: 99%

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

Knop

Vilsbøll²,

Larsen³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

100

View full text Add to dashboard Cite

show abstract

“…Coordinated gastric contractions and secretion of hydrochloric acid and pepsinogen cause the mechanical and enzymatic disintegration of food which becomes the chymus [16]. The stomach also participates in the regulation and modulation of the digestive function of the pancreas, especially influencing exocrine pancreatic enzymes secretion [17,18].…”

Section: Introductionmentioning

confidence: 99%