Ornithine decarboxylase (ODC) activity has been found to be preferentially associated with small intestinal villus cells rather than crypt cells in the rat. In the present study, ODC, S-adenosylmethionine decarboxylase (SAMDC), and polyamines were measured in isolated enterocytes to determine which cell populations increased polyamine biosynthetic activity after refeeding. Two hours following refeeding, significant increases in ODC were observed in villus tip (10 times) and midvillus (20 times) enterocytes. No increase in ODC activity was found in isolated crypt cells. A similar pattern was observed for SAMDC. Enzyme activity increased in villus tip (2 times) and midvillus (27 times) cells but not in crypt enterocytes. Putrescine contents were increased following refeeding in midvillus enterocytes (P less than 0.05) and in crypt cells (P less than 0.05). The accumulation of putrescine in midvillus cells occurs via ODC-induced biosynthesis, whereas in crypt enterocytes it may be due to putrescine uptake. The lack of induction of ODC and SAMDC in crypt enterocytes following acute refeeding suggests these enzymes are apparently not involved in the initiation of cell proliferation known to occur under this condition.
The effects of inhibiting polyamine synthesis on the functional development of the gastric mucosa were studied in rats from 5 to 40 days old. They were treated from day 14 after birth with alpha-difluoromethylornithine (DFMO) at a concentration of 2% in the drinking water of mothers and pups. The rats were weaned on day 18. Basal acid and pepsin secretion, oxyntic gland mucosal pepsinogen content, and antral gastrin content followed similar developmental patterns in control animals. Levels of these parameters remained measurable but low until around the time of weaning, when dramatic log linear rises were observed. DFMO failed to delay the onset of the rises in any of these maturational indices. Ornithine decarboxylase (ODC) activity in the oxyntic gland mucosa was low but discernible in rats of every age studied. DFMO significantly reduced ODC activity at every age except 40 days, where there was no difference from control values. Our results suggest that ODC activity in the rat gastric mucosa does not change appreciably during neonatal development and that inhibiting putrescine synthesis from its precursor ornithine by DFMO treatment does not prevent or delay gastric mucosal maturation.
Refeeding fasted rats with normal rat food and with a variety of amino acids increases ornithine decarboxylase (ODC) activity considerably. The time course of that increase, the areas of the digestive tract directly affected, and the effective concentrations of stimulants are unknown. By use of isolated 5-cm segments of rat jejunum, we determined that maximal activation of ODC occurred after a 2-h exposure to 0.6 M glycine. Increased activity was first apparent after a 1-h exposure to glycine and was significant after a 2-h exposure to 0.05 M glycine. ODC activity increased the most in segments of jejunum, followed by segments of ileum and then duodenum. Glycine (0.4 M) failed to increase ODC activity in gastric and colonic mucosa. Interestingly, D-alanine was more effective than L-alanine in stimulating ODC activity in the jejunum. Enzyme activity was not dependent on osmotic activity of the test substances. Glucose increased enzyme activity, but mannitol and fructose were without effect. The effects of glycine were significantly greater than those of glucose. In summary, ODC of the small intestinal mucosa is increased by direct contact with amino acids and glucose within 2 h after exposure. Increased enzyme activity depends on the nature of the stimulant rather than the osmotic activity of the solution in contact with the mucosa.
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