| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Internal Medicine, Yale University, New Haven, CT, USA
2 Department of Cellular and Molecular Physiology, Yale University, New Haven, CT, USA; Department of Surgery, Yale University, New Haven, CT, USA
3 Department of Internal Medicine, Yale University, New Haven, CT, USA; Department of Cellular and Molecular Physiology, Yale University, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: henry.binder{at}yale.edu.
Luminal iso-butyrate, a relatively poor metabolized short chain fatty acid (SCFA), induces HCO3 secretion via a Cl-independent, DIDS-insensitive, carrier-mediated process as well as inhibiting both Cl-dependent and cAMP-induced HCO3 secretion. The mechanism(s) responsible for these processes have not been well characterized. HCO3 secretion was measured in isolated colonic mucosa mounted in lucite chambers using pH stat technique and during microperfusion of isolated colonic crypts. 14C-butyrate, 14C-iso-butyrate and 36Cl uptake was also determined by apical membrane vesicles (AMV) isolated from surface and/or crypt cells. Butyrate stimulation of Cl-independent, DIDS-insensitive, NPPB-insensitive HCO3 secretion is greater than that by iso-butyrate suggesting that both SCFA transport and metabolism are critical for HCO3 secretion. Both lumen and serosal 25 mM butyrate inhibit cAMP-induced HCO3 secretion to a comparable degree (98% vs 90%). In contrast, Cl-dependent HCO3 secretion is down-regulated by lumen 25 mM butyrate considerably more than by serosal butyrate (98% vs 37%). Butyrate did not induce HCO3 secretion in isolated microperfused crypts while an outward directed HCO3 gradient-driven induced 14C-butyrate uptake by surface, but not crypt cell AMV. Both 36Cl- HCO3 exchange and potential-dependent 36Cl movement in AMV were inhibited by 96-98% by 20 mM butyrate. We conclude: a) SCFA-dependent HCO3 secretion is the result of SCFA transport across the apical membrane via a SCFA-HCO3 exchange more than intracellular SCFA metabolism. b) SCFA-dependent HCO3 secretion is most likely a result of an apical membrane SCFA-HCO3 exchange in surface epithelial cells. c) SCFA down-regulates Cl-dependent and cAMP-induced HCO3 secretion secondary to SCFA inhibition of apical membrane Cl-HCO3 exchange and anion channel activity, respectively.
This article has been cited by other articles:
|
|
 |
|
  B. H. Bajka, J. M. Clarke, L. Cobiac, and D. L. Topping Butyrylated starch protects colonocyte DNA against dietary protein-induced damage in rats Carcinogenesis, November 1, 2008; 29(11): 2169 - 2174. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. B. Subramanya, V. M. Rajendran, P. Srinivasan, N. S. Nanda Kumar, B. S. Ramakrishna, and H. J. Binder Differential regulation of cholera toxin-inhibited Na-H exchange isoforms by butyrate in rat ileum Am J Physiol Gastrointest Liver Physiol, October 1, 2007; 293(4): G857 - G863. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Donowitz and X. Li Regulatory Binding Partners and Complexes of NHE3 Physiol Rev, July 1, 2007; 87(3): 825 - 872. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Zhang, N. Ameen, J. E. Melvin, and S. Vidyasagar Acute inflammation alters bicarbonate transport in mouse ileum J. Physiol., June 15, 2007; 581(3): 1221 - 1233. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. C. Roy, C. L. Kien, L. Bouthillier, and E. Levy Short-Chain Fatty Acids: Ready for Prime Time? Nutr Clin Pract, August 1, 2006; 21(4): 351 - 366. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
