Publikationsdatenbank

Bicarbonate-dependent and bicarbonate-independent mechanisms contribute to nondiffusive uptake of acetate in the ruminal epithelium of sheep. (2009)

Art

Zeitschriftenartikel / wissenschaftlicher Beitrag

Autoren

Aschenbach, J. R.

Bilk, S.

Tadesse, G.

Stumpff, F.

Gäbel, G.

Quelle

American journal of physiology : Gastrointestinal and liver physiology

Bandzählung: 296

Heftzählung: 5

Seiten: G1089 – G1107

ISSN: 0193-1857

Sprache

Englisch

Verweise

URL (Volltext): http://ajpgi.physiology.org/cgi/reprint/90442.2008v1

Pubmed: 19264953

Kontakt

Institut für Veterinär-Physiologie

Oertzenweg 19 b
14163 Berlin
+49 30 838 62600
physiologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

The present study investigated the significance of apical transport proteins for ruminal acetate absorption and their interaction with different anions. When performing anion competition experiments in the washed reticulo-rumen, chloride disappearance rate (initial concentration, 28 mM) was inhibited by the presence of a SCFA mixture (15 or 30 mM of each acetate, propionate and butyrate). Disappearance rates of acetate and propionate, but not butyrate, (initial concentration, 25 mM each) were diminished by 40 mM or 80 mM chloride. In isolated ovine ruminal epithelia mounted in Ussing chambers, an increase in chloride concentration from 4.5 mM to 90 mM led to a decrease of apical acetate uptake at a concentration of 0.5 mM. Mucosal nitrate inhibited acetate uptake most potently while sulphate had no effect. Decreasing mucosal pH from 7.4 to 6.1 approximately doubled uptake of acetate both at 0.5 and 10 mM; but this doubling was almost abolished when HCO3(-) was absent. The stimulated uptake at mucosal pH 6.1 consisted of a bicarbonate-dependent, nitrate-inhibitable part (Km = 54 mM) and a bicarbonate-independent component (Km = 12 mM) that was also sensitive to nitrate inhibition. Maximal uptake was three times larger for bicarbonate-dependent vs. bicarbonate-independent uptake. Mucosal addition of 200 microM diisothiocyanatostilbene 2,2-disulfonic acid (DIDS), 400 microM p-chloromercuribenzene sulfonic acid (pCMBS), 800 microM p-hydroxymercuribenzoic acid (pHMB) or 100 microM phloretin had no effects on acetate uptake although the latter two inhibited L-lactate uptake. Our data conclusively show a dominant involvement of proteins in apical acetate uptake. Previously described pH effects on acetate absorption originate mainly from modulation of acetate/bicarbonate exchange. Additionally, there is bicarbonate-independent uptake of acetate anions that is protein-coupled but not via monocarboxylate cotransporter (MCT). Key words: anion exchanger, bicarbonate transport, short chain fatty acids, forestomach.