Intraluminal calcium binding does not mediate fatty acid-induced pancreatic bicarbonate secretion

Since the chain length dependency of fatty acid-induced pancreatic exocrine secretion parallels that of fatty acid-induced inhibition of gastric emptying, similar mechanisms of action may be involved. An earlier study suggested that binding of calcium might mediate fatty acid-induced inhibition of gastric emptying. This study investigated possible mediation of fatty acid-induced pancreatic secretion by calcium binding. Pancreatic secretory response to intraduodenal administration of dodecanoate and various calcium chelators (sodium EDTA, calcium-saturated EDTA, sodium dodecyl sulfate, sodium dioctyl sulfosuccinate, and sodium taurocholate) was studied in three dogs equipped with chronic pancreatic fistulae. Calcium affinity of the various test solutions was quantitated by titrating aliquots of perfusate against a standard CaCl2 solution. Sodium EDTA was found to be the most potent calcium binder (pKc 8.3); sodium dodecanoate, sodium dodecyl sulfate, and sodium dioctyl sulfosuccinate were moderate calcium binders (pKc 7.3, 7.2, 6.9, respectively), whereas sodium taurocholate and calcium-saturated EDTA were poor calcium binders. Sodium dodecanoate evoked brisk bicarbonate output (0.6-1.6 mEq/15 min). Minimal secretory responses were observed in response to all other agents tested. These findings suggest that calcium binding is not involved in mediation of fatty acid-induced pancreatic bicarbonate secretion.