Pancreatic Secretory Trypsin Inhibitor in Human Gastrointestinal Epithelia and Gastric Juice

Freeman, TC; Playford, RJ; Beardsall, Kathryn; Francis-Reme, ML; Levi, S; Calam, J.

doi:10.1042/cs076009pa

Cited by 2 publications

(3 citation statements)

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“…3-1 (2-1-5-0) EGF secretion (pmollhour) (1-7-11i5) 6 The main study Eighteen ofthe 140 samples were rejected because they contained bilirubin or trypsin; four from each of the aspiration, saline perfusion, and initial bicarbonate periods and two from each of the bicarbonate plus misoprostol and final bicarbonate periods. Measured gastric output of PSTI was mean (range) 2 (1-3) ,tg/hour during simple aspiration, 4 (3)(4)(5) FIgIhour during perfusion with saline, and rose to a plateau of 11 (8-45) mg/hour during the first bicarbonate period. Gastric secretion of PSTI remained at 11 (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21) pg/hour (NS) when bicarbonate perfusion was continued without misoprostol for a further 40 minutes in four subjects.…”

Section: Effects Of Misoprostol Laboratory Analysesmentioning

confidence: 98%

“…Pancreatic secretory trypsin inhibitor (PSTI) is a potent inhibitor of trypsin and chymotrypsin' that has recently been found in the foveolar cells of the stomach as well as in the pancreas.2 3 The foveolar cells also secrete mucus,4 which helps to create the protective gastric mucus layer. 5 We therefore speculated that PSTI may protect the gastric mucus layer from damage by pancreatic proteases that reflux into the stomach in normal people and, to a greater extent, in diseases including chronic gastric ulcer.…”

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confidence: 99%

“…3 We therefore measured gastric PSTI both before and during intragastric neutralisation with bicarbonate. Epidermal growth factor was measured as a control protein of similar size to PSTI, present in gastric juice, but principally of salivary origin.…”

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confidence: 99%

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Gastric output of pancreatic secretory trypsin inhibitor is increased by misoprostol.

Batten

Freeman

Beardshall

et al. 1991

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Pancreatic secretory trypsin inhibitor (PSTI) is a potent protease inhibitor that also has growth promoting activity. It has recently been identified in the foveolar cells of the stomach, which secrete mucus. We examined the effects of the prostaglandin E1 analogue misoprostol on gastric PSTI output. Seven normal volunteers took part. An initial period ofgastric aspiration was followed by four 40 minute periods of gastric perfusion at 5 ml/minute of: 0-14 molll saline, 0.17 mmol/l bicarbonate, bicarbonate with misoprostol 400 rig, and then bicarbonate again. All perfusates contained polyethylene glycol 4000 as a marker. Misoprostol increased median gastric secretion of PSTI from 11 to 33 ig/hour (p<005), producing concentrations in gastric juice six times higher than those found in jejunal juice and about 1/30 of the values seen in pancreatic juice. Median mucus secretion increased to a lesser extent from 29 to 38 mg/hour during misoprostol. There was no change in intragastric concentrations of protein or of epidermal growth factor during infusion of misoprostol. Infusion of pentagastrin (6 iglkg/ hour) had no effect on gastric secretion of mucus, PSTI, or protein. Human gastric mucus was degraded on incubation with trypsin in vitro and this was prevented by the addition of PSTI. These results suggest that gastric PSTI may protect the gastric mucus layer against refluxed pancreatic proteases. Increased output of PSTI during microprostol may contribute to the protective effect of this drug.

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