Pancreatic bicarbonate response to food-bound hydrogen ion along the gut.

Recent reports suggest most solid food enters the duodenum as small particles. Our studies showed that small particles of liver were capable of binding hydrogen ions (H+), but there was slow equilibration of H+ between particulate and aqueous phases. We wondered whether titratable acid as H+ bound to meat particles could effectively stimulate pancreatic bicarbonate secretion despite slow diffusion. We studied mongrel dogs with chronic pancreatic fistulas; the intestinal lumen was washed free of endogenous pancreatic enzymes. Pancreatic bicarbonate and protein responses were measured during duodenal perfusion with pH 2 or pH 3 gels that delivered 1, 2, or 4 mEq/15 min of titratable acid (endpoint pH 4.5). Gels consisted of acidified, 0.1-0.7-mm particles of beef liver or bovine serum albumin or lactic acid suspended with 2% starch in 0.15 M NaCl. The liver, bovine serum albumin, and lactate had similar titration curves. At pH 2 or pH 3, liver particles were about as effective as bovine serum albumin in stimulating pancreatic bicarbonate secretion. Likewise, pH 3 liver particles were equipotent with pH 3 lactate on pancreatic bicarbonate secretion when both perfusates were allowed access to the whole intestine. However, when confined to the first 45 cm of proximal intestine, much less H+ was dissipated from the liver versus the lactate; and, correspondingly, there was a much greater decrement in pancreatic bicarbonate secretion from whole gut responses with liver versus lactate. We conclude that titratable acid bound to solid food particles is a potent stimulus of pancreatic bicarbonate secretion despite its slow diffusion. Our studies suggest that H+ slowly diffusing from particles excites pancreatic bicarbonate secretion by triggering H+ receptors along more distal intestine.