title: Diet-induced regulation of bitter taste receptor subtypes in the mouse gastrointestinal tract.
abstract: Bitter taste receptors and signaling molecules, which detect bitter taste in the mouth, are expressed in the gut mucosa. In this study, we tested whether two distinct bitter taste receptors, the bitter taste receptor 138 (T2R138), selectively activated by isothiocyanates, and the broadly tuned bitter taste receptor 108 (T2R108) are regulated by luminal content. Quantitative RT-PCR analysis showed that T2R138 transcript is more abundant in the colon than the small intestine and lowest in the stomach, whereas T2R108 mRNA is more abundant in the stomach compared to the intestine. Both transcripts in the stomach were markedly reduced by fasting and restored to normal levels after 4 hours re-feeding. A cholesterol-lowering diet, mimicking a diet naturally low in cholesterol and rich in bitter substances, increased T2R138 transcript, but not T2R108, in duodenum and jejunum, and not in ileum and colon. Long-term ingestion of high-fat diet increased T2R138 RNA, but not T2R108, in the colon. Similarly, α-gustducin, a bitter taste receptor signaling molecule, was reduced by fasting in the stomach and increased by lowering cholesterol in the small intestine and by high-fat diet in the colon. These data show that both short and long term changes in the luminal contents alter expression of bitter taste receptors and associated signaling molecules in the mucosa, supporting the proposed role of bitter taste receptors in luminal chemosensing in the gastrointestinal tract. Bitter taste receptors might serve as regulatory and defensive mechanism to control gut function and food intake and protect the body from the luminal environment.
authors.affiliation: CURE Digestive Diseases Research Center, Digestive Diseases Division, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America.
authors.forename: Gaia
authors.initials: G
authors.lastname: Vegezzi
authors.affiliation: CURE Digestive Diseases Research Center, Digestive Diseases Division, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America.
authors.forename: Laura
authors.initials: L
authors.lastname: Anselmi
authors.affiliation: CURE Digestive Diseases Research Center, Digestive Diseases Division, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America.
authors.forename: Jennifer
authors.initials: J
authors.lastname: Huynh
authors.affiliation: Department of Pharmacy, University of Parma, Parma, Italy.
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Barocelli
authors.affiliation: CURE Digestive Diseases Research Center, Digestive Diseases Division, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America; Veterans Administration, Greater Los Angeles Health system, Los Angeles, California, United States of America.
authors.forename: Enrique
authors.initials: E
authors.lastname: Rozengurt
authors.affiliation: Department of Anatomy, Physiology, & Cell Biology, School of Veterinary Medicine, University of California Davis, Davis, California, United States of America.
authors.forename: Helen
authors.initials: H
authors.lastname: Raybould
authors.affiliation: CURE Digestive Diseases Research Center, Digestive Diseases Division, Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America; Department of Neurobiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America; Veterans Administration, Greater Los Angeles Health system, Los Angeles, California, United States of America.
authors.forename: Catia
authors.initials: C
authors.lastname: Sternini
mesh_terms: D000818:Animals; D003106:Colon / Q000378:metabolism; D004032:Diet; D059305:Diet, High-Fat; D004386:Duodenum / Q000378:metabolism; D005215:Fasting; D005753:Gastric Mucosa / Q000378:metabolism; D041981:Gastrointestinal Tract / Q000378:metabolism*; D005786:Gene Expression Regulation; D020962:Heterotrimeric GTP-Binding Proteins / Q000378:metabolism; D007082:Ileum / Q000378:metabolism; D007421:Intestine, Small / Q000378:metabolism; D007583:Jejunum / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger; D060888:Real-Time Polymerase Chain Reaction; D043562:Receptors, G-Protein-Coupled / Q000235:genetics* / Q000378:metabolism* / Q000502:physiology; D015398:Signal Transduction; D013649:Taste; D000098706:Taste Receptors, Type 2
chemical_list: D012333:RNA, Messenger; D043562:Receptors, G-Protein-Coupled; C000598592:T2R138 protein, mouse; C560578:Tas2R108 protein, mouse; D000098706:Taste Receptors, Type 2; C524407:GNAT3 protein, mouse; D020962:Heterotrimeric GTP-Binding Proteins