Pathophysiological role of cholecystokinin in humans.
Level 5 - mechanism / opinion, no new human data
Narrative review of human and animal mechanisms without systematic search methodology
PubMed 10759224 · doi:10.1046/j.1440-1746.2000.02178.x
What was done
This narrative review summarizes physiological mechanisms regulating cholecystokinin (CCK) secretion—including intestinal releasing factors, pancreatic monitor peptide, and intraluminal bile acid feedback—and examines CCK alterations in acute and chronic human pancreatitis.
What was found
The abstract reports qualitative physiological relationships without numerical data or effect sizes. Bile exclusion from the duodenum increases basal and stimulated plasma CCK release, which is reversed by bile salt replacement. In acute pancreatitis, plasma CCK is elevated specifically in gallstone pancreatitis, but not in alcoholic or idiopathic etiologies. Patients with chronic pancreatitis and mild-to-moderate exocrine dysfunction have elevated plasma CCK concentrations, whereas patients with advanced pancreatic insufficiency exhibit reduced CCK responses to a test meal compared to healthy controls.
Why it matters
The paper outlines how disrupted bile flow and exocrine feedback may create a cycle of excessive CCK release that worsens pancreatic injury, providing a theoretical rationale for testing CCK-A receptor antagonists in acute pancreatitis.
Limits
As a narrative review, it lacks systematic search criteria, quality appraisal, and pre-specified inclusion methods. Findings synthesize findings from both rodent models (such as isolated monitor peptide) and human studies without providing sample sizes, quantitative estimates, or confidence intervals in the abstract.
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