To better understand the mechanism of phosphatidylcholine synthesis in the stomach, [
3H] choline incorporation into phosphatidylcholine in response to the drugs which have been commonly used for treating the patients with gastric ulcer was examined using isolated guinea pig gastric glands.
Teprenone stimulated [
3H] choline incorporation into phosphatidylcholine in gastric glands, up to 146±11% of control (n=6, P<0.05).
On the other hand famotidine, ranitidine and cimetidine significantly decreased the incorporation to 73±8%, 72±11%, 67±11% of control, respectively (n=6, P<0.05, P<0.05, P<0.05). When the glands were pulsed with [
3H] choline followed by incubation in the presense of teprenone or each H
2RA for 180min to see the effects of the agents on the limiting step of the phosphatidylcholine synthesis, teprenone also significantly stimulated [
3H] choline incorporation into phosphatidylcholine, but each H
2RA did not affect phosphatidylcholine biosynthesis any more.
Teprenone stimulated CTP: phosphocholine cytidylyltransferase (CTF) from a basal value of 0.92 ±0.10 to 1.69±0.39 (nmol/min/mg protein) (n=3, P<0.05).
These results suggest that teprenone may stimulate phosphatidylcholine biosynthesis through the activation of CTF, a late-limiting enzyme of PC biosynthesis, and H
2RA may affect phosphatidylcholine synthesis by inhibiting choline transport or choline kinase in gastric glands.
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