title: No negative feedback regulation between plasma CCK levels and luminal tryptic activities in patients with pancreatic insufficiency.
abstract: The study was conducted on five healthy subjects and six patients with calcifying pancreatitis (CP) and steatorrhea. Following overnight fasting, one tube each was placed in the stomach and the upper of the small intestine, respectively. Through the gastric tube, a test meal that included 30 g of fat (total calories, 625 kcal, 500 mL) was infused over a span of 30 min. Every 30 min (up to 150 min), fluid samples in the upper small intestine were collected and chilled, and the amylase, trypsin, and lipase levels were determined. In addition, in the case of the CP patients, a high-potency pancreatin preparation was infused into the stomach together with the test meal. In order to determine the plasma CCK level, blood sample were collected before test meal infusion and at 10, 20, 30, 45, 60, 90, 120, and 150 min subsequent to infusion. The plasma CCK was extracted using a Sep-Pak C-18 cartridge and analyzed with radioimmunoassay using an OAL-656 antibody. The result was converted to the CCK-8 level and expressed in pg/mL. The enzyme activities in the upper small intestine of the CP patients after test meal administration amounted to 22.8 (amylase), 10.8 (trypsin), and 16.9% (lipase) compared with the corresponding figures for the normal subjects. Following administration of a high-potency pancreatin in patients with CP, enzyme activities in the upper small intestine increased to 132.2 (amylase), 38.7 (trypsin), and 45.3% (lipase) compared with levels in the normal subjects. However, the healthy subjects and the CP patients, both with and without treatment with supplementary exogenous enzymes, all exhibited similar profiles in the plasma CCK response to stimuli. Based on these findings, we concluded that a negative feedback mechanism does not exist between the tryptic activity of the upper small intestine and the CCK secretory response in patients with chronic pancreatitis.
authors.affiliation: Third Department of Internal Medicine, Hirosaki University School of Medicine, Aomori, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: K
authors.initials: K
authors.lastname: Takebe
authors.forename: K
authors.initials: K
authors.lastname: Kudoh
authors.forename: M
authors.initials: M
authors.lastname: Ishii
authors.forename: K
authors.initials: K
authors.lastname: Imamura
authors.forename: H
authors.initials: H
authors.lastname: Kikuchi
authors.forename: F
authors.initials: F
authors.lastname: Kasai
authors.forename: Y
authors.initials: Y
authors.lastname: Tandoh
authors.forename: N
authors.initials: N
authors.lastname: Yamada
authors.forename: Y
authors.initials: Y
authors.lastname: Arai
mesh_terms: D000328:Adult; D000681:Amylases / Q000378:metabolism; D002766:Cholecystokinin / Q000097:blood*; D002908:Chronic Disease; D010188:Exocrine Pancreatic Insufficiency / Q000378:metabolism*; D005246:Feedback / Q000502:physiology; D005502:Food; D006801:Humans; D007421:Intestine, Small / Q000201:enzymology*; D008049:Lipase / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010194:Pancreatin / Q000008:administration & dosage; D010195:Pancreatitis / Q000378:metabolism*; D014357:Trypsin / Q000378:metabolism*
chemical_list: D010194:Pancreatin; D002766:Cholecystokinin; D008049:Lipase; D000681:Amylases; D014357:Trypsin