| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Anatomy, Physiology and Cell Biology
2 Center for Comparative Medicine, UC Davis School of Veterinary Medicine, Davis, CA, USA
3 Department Pathology and Laboratory Medicine, University of Cincinnati, OH, USA
Long chain triglyceride (>C12) in the intestinal lumen potently inhibits gastric emptying and acid secretion via the vagal afferent pathway. While the mechanism of inhibition involves the formation of chylomicrons, the essential role of the apolipoprotein apo A-IV is unclear. Using apo A-IV–/– mice, we tested the hypothesis that inhibition of gastric emptying and gastric acid secretion in response to dietary lipid is dependent upon apo A-IV. As measured by nuclear scintigraphy in awake mice, gastric emptying of an ingested whole-egg meal was significantly faster in apo A-IV–/– knockout versus A-IV+/+ controls (34 ± 1 versus 54 ± 3 min, P < 0.0001). In anaesthetized A-IV+/+ mice, meal-stimulated gastric acid secretion was 59% inhibited by intestinal lipid infusion; this was abolished in apo A-IV–/– mice. Oral gavage of lipid in awake mice activated neurones throughout the nucleus of the solitary tract (NTS) in A-IV+/+ mice, measured by immunohistochemical localization of Fos protein expression. However, in the mid region of the NTS (bregma –7.32 to –7.76 mm), Fos expression in response to intestinal lipid was significantly decreased by 50% in apo A-IV–/– mice compared to A-IV+/+ controls. We conclude that activation of the vagal afferent pathway and inhibition of gastric function in response to dietary lipid is partly dependent upon apo A-IV.
(Received 27 August 2005;
accepted after revision 13 October 2005;
first published online 20 October 2005)
Corresponding author H. E. Raybould: 1321 Haring Hall, Vet Med: APC, UC Davis School of Veterinary Medicine, Davis, CA 95616, USA. Email: heraybould{at}ucdavis.edu
This article has been cited by other articles:
|
|
 |
|
  S. Hao, C. Sternini, and H. E. Raybould Role of CCK1 and Y2 receptors in activation of hindbrain neurons induced by intragastric administration of bitter taste receptor ligands Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2008; 294(1): R33 - R38. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. L. Whited, P. Tso, and H. E. Raybould Involvement of Apolipoprotein A-IV and Cholecystokinin1 Receptors in Exogenous Peptide YY3 36-Induced Stimulation of Intestinal Feedback Endocrinology, October 1, 2007; 148(10): 4695 - 4703. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. L. Whited, D. Thao, K. C. K. Lloyd, A. S. Kopin, and H. E. Raybould Targeted disruption of the murine CCK1 receptor gene reduces intestinal lipid-induced feedback inhibition of gastric function Am J Physiol Gastrointest Liver Physiol, July 1, 2006; 291(1): G156 - G162. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
