<b>STIMULATION OF INTESTINAL CHOLECYSTOKININ SECRETION BY FREE FATTY ACID IN RATS IS NOT ASSOCIATED WITH </b><b>AN INCREASE IN THE CCK mRNA LEVEL </b>
TL;DRAbstract
Sodium oleate (0.25 mmol/kg -h), synthetic trypsin inhibitor (camostat mesilate, 40 mg/ kg -h), or saline was intraduodenally given to rats during 24 h. Trypsin inhibitor applied for 24 h elevated the level of both plasma cholecystokinin (CCK) and intestinal CCK mRNA. Sodium oleate also increased the plasma CCK level during 24 h. Despite the increase in plasma CCK, sodium oleate did not alter the level of duodenal CCK mRNA. The results contrast with the previous demonstration that the stimulation of CCK release by an ordinary rat chow or trypsin inhibitor is associated with an increase in the level of intestinal CCK mRNA. We conclude that stimulation of CCK secretion is not necessarily linked with an increase in the CCK mRNA level.
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Sodium oleate (0.25 mmol/kg -h), synthetic trypsin inhibitor (camostat mesilate, 40 mg/ kg -h), or saline was intraduodenally given to rats during 24 h. Trypsin inhibitor applied for 24 h elevated the level of both plasma cholecystokinin (CCK) and intestinal CCK mRNA. Sodium oleate also increased the plasma CCK level during 24 h. Despite the increase in plasma CCK, sodium oleate did not alter the level of duodenal CCK mRNA. The results contrast with the previous demonstration that the stimulation of CCK release by an ordinary rat chow or trypsin inhibitor is associated with an increase in the level of intestinal CCK mRNA. We conclude that stimulation of CCK secretion is not necessarily linked with an increase in the CCK mRNA level.
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