128 Assessment of the presence of chemosensing receptors based on bitter and fat taste in the gastrointestinal tract of young pig 1 M. Colombo, P. Trevisi, G. Gandolfi, and P. Bosi 2 University of Bologna, DIPROVAL, 42123 Reggio Emilia, Italy 1 This research was funded by the European Union Seventh Framework Program (FP7 ⁄ 2007–2013) under the grant agreement no. 227549. 2 Corresponding author: paolo.bosi@unibo.it ABSTRACT: Knowledge on porcine bitter and fat taste receptors and on their expression in gastrointestinal tract of pigs is scarce. We searched for the presence of porcine homologous sequences for 13 human transcripts of bitter and fat taste receptors in ENSEMBL and National Center for Biotechnology Information databases. For taste 2 receptor (TAS2R) 8, alignment was not observed; for TAS2R13 and TAS2R46 the porcine predicted sequence aligned with several other human bitter genes. For 7 genes for bitter taste (TAS2R1, TAS2R3, TAS2R7, TAS2R9, TAS2R10, TAS2R16, and TAS2R38) and for 3 genes for fat taste (GPR40, GPR43, and GPR120), a full homology for exon sequences was found and primers were designed by Primer3. These 7 genes were amplified with real-time PCR and verified on agarose gel in 5 gastrointestinal segments of weaned pigs: oxyntic (ST1), pyloric (ST2), and cardiac to oxyntic transition mucosa (ST3), jejunum (JEJ), and colon (COL). Suitability of mRNA was verified by amplifying RPL4 and HMBS2 genes. Each bitter taste gene was detectable on agarose gel in at least 1 subject of all the gastrointestinal segments except for TAS2R3 and TAS2R38 that were never detected in ST1 and COL, respectively. The inspection of bitter taste genes amplification curve indicated that the expression was in general very low. GPR43 and GPR120 were present in all segments from all pigs. Expression was not detected for GPR40. Data also indicate that colon is the preeminent tract where fat detection by GPR120 takes place (P < 0.001). The presence of gene expression for several chemosensing receptors for bitter and fat taste in different compartments of the stomach confirms that this organ should be considered a player for the early detection of bolus composition. Key words: bitter, fat, pig, stomach, taste receptor © 2012 American Society of Animal Science. All rights reserved. J. Anim. Sci. 2012.90:128–130 doi:10.2527/jas53793 INTRODUCTION Humans recognize sweet, umami, sour, salty, and bitter, and novel tastes have been described such as fat taste and metallic (Chaudhari and Roper, 2010). Recent research indicates that the presence of chemosensing receptors for bitter and fat taste is not restricted to the mouth but is extended to other organs and tissues. Particularly, their location along the whole digestive tract contributes to the control of secreting activity, regulation of several hormones, and afferent neuronal modulation. In pigs, the taste chemosensory system has been investigated for its impact on the feed preference and feed intake (Roura and Tedò, 2009). The diffuse gastrointestinal chemosensory system consists of solitary chemosensory cells that express molecules of the chemoreceptorial cascade activated by G protein- coupled receptors (GPR) and α-gustducin interaction (Iwatsuki and Torii, 2012). Taste 2 receptors (TAS2R) are the GPR identified as receptor for bitter taste. Bitter taste is initiated by a large number of different and unrelated organic molecules recognized by a broad range of receptors of the TAS2R family; humans have 25 functional bitter taste receptors genes. Other GPR have been identified in taste buds and likely contribute to the detection of nutrients. These include GPR40, GPR43, and GPR120 genes, which are expressed in subsets of taste cells and detect fatty acids (Cartoni et al., 2010). To date, we are not aware of any study that investigated TAS2R or GPR genes in pigs. The goal of this study was to assess the presence of porcine homologous sequences for the known human transcripts of bitter and fat taste receptors in different segments of the gastrointestinal tract of the young pigs. Published January 23, 2015