Pentagastrin induction of spermine/spermidine N1-acetyltransferase and mucosal polyamines

The trophic response of the gastrointestinal mucosa to treatment with the hormone gastrin includes a polyamine-dependent step. Because gastrin does not induce ornithine decarboxylase, experiments were designed to determine whether pentagastrin induced the polyamine interconverting enzyme, spermine/spermidine N1-acetyltransferase (SAT). Eight hours after intraperitoneal treatment of rats with either spermidine (0.8 mmol/kg) or pentagastrin (250 micrograms/kg) oxyntic gland mucosal SAT activity was increased from roughly 400 to 800 pmol [14C]acetate.mg protein-1.h-1. In contrast, colonic mucosa was not sensitive to pentagastrin even though spermidine treatment induced nearly a 400% increase in SAT activity. Measurement of both oxyntic gland and colonic mucosal polyamine concentrations showed that by 16 h after pentagastrin (250 micrograms/kg ip) putrescine, acetylspermidine, and spermidine levels all were increased to a level approximately 200% of that observed in NaCl-treated rats. By 24 h mucosal polyamine content of pentagastrin-treated rats was not different from control. Essentially the same results were found in animals treated with difluoromethylornithine, thus demonstrating that the increase in mucosal polyamine concentration was not related to the induction of ornithine decarboxylase. The results of these experiments demonstrate that unlike most hormones, the hormone gastrin induces the polyamine converting enzyme, SAT, rather than ornithine decarboxylase during stimulation of polyamine-dependent cell growth and/or division.