Abstract
After the development of reliable, highly sensitive, specific radioimmunologic methods for measuring physiologic CCK concentrations in human plasma, we have been able to study the importance of CCK in the postprandial activation of pancreatic enzyme secretion. In man, food causes a threefold increase in the basal plasma CCK concentration with a peak at about 60 minutes. The highest CCK concentrations are observed after intraduodenal fat infusion. Selective proximal vagotomy results in a significant increase in basal CCK concentrations in duodenal ulcer patients without altering the postprandial CCK output. After gastric resection (Billroth I or Billroth II) an initial greater postprandial CCK output is observed. In patients with chronic pancreatic insufficiency without enzyme substitution, basal plasma CCK concentrations and the early postprandial CCK output were elevated which indicated a feedback mechanism between pancreatic enzyme secretion and CCK release from the mucosa of the upper small intestine.
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