Pentagastrin increases pepsin secretion without increasing its
fractional synthetic rate.
Corbett, Mary E., Eric J. S. Boyd, James G. Penston, Kenneth G.
Wormsley Peter W. Watt, and Michael J. Rennie.
Department of Anatomy & Physiology, University of Dundee,
Department of Clinical Pharmacology, Ninewells Hospital & Medical
School, Dundee
APStracts 2:0068E, 1995.
We have studied the effects of increasing doses of pentagastrin on
gastric secretion of pepsin, and on incorporation of L-[1-13C]leucine
into gastric aspirate protein as an index of pepsin synthesis.
Pentagastrin (0.25-4.0 [mu]g.kg-1.h-1) significantly increased pepsin
output from basal 76 mg.h-1 to up to 181 mg.h-1, but did not
significantly alter incorporation of L-[1-13C]leucine from the basal
fractional synthetic rate of 3.63 +/- 0.05 %.h-1. In 4 subjects in
whom infusion of tracer leucine was continued for over 1 day,
aspiration of pepsin between 24 and 27 h demonstrated that plateau
13C-labelling of leucine in pepsin had been attained, but at a value
which was only 48% of the 13C-labelling of plasma [alpha]-KIC (0.730
+/- 0.02 vs 1.520 +/- 0.14 APE (means +/- SEM)). This suggests that
actual rates of pepsin synthesis were approximately double those
calculated on the basis of [alpha]-KIC labelling. The results are
consistent with an interpretation that increasing doses of
pentagastrin cause increased secretion of pepsinogen by recruitment
of gastric chief cells each synthesising pepsinogen at an unaltered
rate. Plateau 13C-enrichment of [alpha]-KIC may not be a valid
surrogate for plateau 13C-leucine enrichment when calculating
fractional synthetic rates of some secreted proteins.
Received 22 September 1994; accepted in final form 29 March 1995.
APS Manuscript Number E389-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 19 April 1995.