PMID- 9057189 OWN - NLM STAT- MEDLINE DCOM- 19970619 LR - 20190905 IS - 0885-3177 (Print) IS - 0885-3177 (Linking) VI - 14 IP - 2 DP - 1997 Mar TI - Role of extrinsic innervation in carbohydrate-induced ileal modulation of pancreatic secretion and upper gut function. PG - 166-73 AB - Previously we showed that carbohydrate (CHO) in the ileum slowed gastric emptying and increased pancreatic amylase secretion relative to that of other enzymes. Our aim here was to determine if extrinsic innervation of the jejunoileum participates in the CHO-induced ileal modulation of postprandial upper gut function. Six dogs were studied before and 2-3 weeks after in situ neural isolation of the jejunoileum (complete extrinsic denervation). Gastric emptying (GE) and pancreatic amylase secretion were quantitated for 4 h after a 300-ml meal containing 3H-PEH (liquid marker) and 99mTc sulfur colloid cooked with eggs (solid marker). Coincident with feeding, we started a distal ileal infusion of 150 mM NaCl or 40 mg.min-1 CHO. Extrinsic denervation abolished the slowing of GE of liquids and solids and the augmented increase in amylase and trypsin in relation to solid emptying seen in the neurally intact dogs prior to denervation. Denervation also abolished the decrease in total pancreatic exocrine secretion in response to ileal CHO. Increases in plasma concentrations of peptide YY (PYY) were correlated temporally with decreased GE of solids and increased exocrine secretion during ileal CHO in neurally intact dogs, but no increases in PYY release occurred after extrinsic denervation. Extrinsic denervation of the jejunoileum abolished the effect of ileal CHO on GE of liquids and solids, the decrease in total amylase secretion during ileal CHO, and the relative increase in enzyme secretion expressed as total enzyme output per percentage solid marker emptied. Extrinsic innervation of the jejunoileum mediates ileal modulation of GE and the relationship of amylase secretion to GE of solids. The mechanism of this effect may be via neurally mediated release of PYY. FAU - Sarr, M G AU - Sarr MG AD - Gastroenterology Research Unit, Mayo Clinic, Rochester, Minnesota 55905, USA. FAU - Foley, M K AU - Foley MK FAU - Winters, R C AU - Winters RC FAU - Duenes, J A AU - Duenes JA FAU - DiMagno, E P AU - DiMagno EP LA - eng GR - DK39337/DK/NIDDK NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Pancreas JT - Pancreas JID - 8608542 RN - 0 (Carbohydrates) RN - 0 (Peptides) RN - 106388-42-5 (Peptide YY) RN - 39379-15-2 (Neurotensin) RN - EC 3.2.1.- (Amylases) RN - EC 3.4.21.4 (Trypsin) SB - IM MH - Amylases/metabolism MH - Animals MH - Carbohydrates/*pharmacology MH - Denervation MH - Dogs MH - Female MH - Gastric Emptying/*physiology MH - Ileum/*innervation/*physiology MH - Jejunum/innervation MH - Kinetics MH - Neurotensin/blood MH - Pancreas/*metabolism MH - Peptide YY MH - Peptides/blood MH - Trypsin/metabolism EDAT- 1997/03/01 00:00 MHDA- 1997/03/01 00:01 CRDT- 1997/03/01 00:00 PHST- 1997/03/01 00:00 [pubmed] PHST- 1997/03/01 00:01 [medline] PHST- 1997/03/01 00:00 [entrez] AID - 10.1097/00006676-199703000-00009 [doi] PST - ppublish SO - Pancreas. 1997 Mar;14(2):166-73. doi: 10.1097/00006676-199703000-00009.