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Possible influence of free fatty acid receptors on pH regulation in the ruminal epithelium of sheep
Author(s) -
Baaske Lisa,
Masur Franziska,
Dengler Franziska,
Rackwitz Reiko,
Kaiser Bastian,
Pfannkuche Helga,
Gäbel Gotthold
Publication year - 2020
Publication title -
journal of animal physiology and animal nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.651
H-Index - 56
eISSN - 1439-0396
pISSN - 0931-2439
DOI - 10.1111/jpn.13308
Subject(s) - amiloride , butyrate , forskolin , epithelium , intracellular ph , receptor , chemistry , medicine , endocrinology , butyric acid , ussing chamber , transepithelial potential difference , biochemistry , biology , intracellular , ion transporter , sodium , organic chemistry , membrane , fermentation , genetics
Abstract High amounts of short‐chain fatty acids (SCFAs) occur in the ovine rumen and constitute the animal's main energy source. However, they lead to an acidification of the ruminal epithelium. Therefore, effective intracellular pH (pH i ) regulation by transport proteins like monocarboxylate transporter 1 (MCT1) and Na + /H + exchangers (NHEs) is pivotal to ruminants to avoid epithelial damage. SCFAs might function not only as nutrients but also as signalling molecules by activating free fatty acid receptors (FFARs) in the ruminal epithelium and thus influence pH i regulation. FFARs work as nutrient sensors, transducing their information by modulating cyclic adenosine monophosphate (cAMP) levels. We hypothesized that (FFAR‐modulated) decreases in cAMP levels stimulate the activity of MCT1 and NHEs in the ruminal epithelium of sheep. We detected two FFARs (GPR109A and FFAR2) immunohistochemically in the ovine ruminal epithelium. Administration of 10 mM butyrate to Ussing chamber‐mounted epithelia provoked a significant reduction in intraepithelial cAMP levels. However, application of the GPR109A agonist niacin did not affect cAMP levels. MCT1 activity was analysed by measuring transepithelial 14 C‐acetate fluxes, which were not inhibited by forskolin‐induced increased cAMP levels. The recovery of pH i after acidification was assessed as an indicator of NHE activity in primary cultured ruminal epithelial cells. Recovery was significantly reduced when cells with increased cAMP levels were subjected to the NHE inhibitor 5‐(N‐ethyl‐N‐isopropyl)‐amiloride (10 µM). Nonetheless, with augmented cAMP levels alone, NHE activity tended to decline. We hypothesize that modulation of cAMP levels by butyrate is accomplished by FFAR2 activation, regulating NHE activity for pH i homoeostasis at least in part.