scholarly journals Gut bitter taste receptor signalling induces ABCB1 through a mechanism involving CCK

2011 ◽  
Vol 438 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Tae-Il Jeon ◽  
Young-Kyo Seo ◽  
Timothy F. Osborne
Keyword(s):  
Bitter Taste ◽  
Taste Receptor ◽  
Physiological Role ◽  
Cell Types ◽  
Enteroendocrine Cells ◽  
Intestinal Cells ◽  
Toxic Substances ◽  
Taste Avoidance ◽  
Dietary Toxins ◽  
Interfering Rna

T2Rs (bitter taste-sensing type 2 receptors) are expressed in the oral cavity to prevent ingestion of dietary toxins through taste avoidance. They are also expressed in other cell types, including gut enteroendocrine cells, where their physiological role is enigmatic. Previously, we proposed that T2R-dependent CCK (cholecystokinin) secretion from enteroendocrine cells limits absorption of dietary toxins, but an active mechanism was lacking. In the present study we show that T2R signalling activates ABCB1 (ATP-binding cassette B1) in intestinal cells through a CCK signalling mechanism. PTC (phenylthiocarbamide), an agonist for the T2R38 bitter receptor, increased ABCB1 expression in both intestinal cells and mouse intestine. PTC induction of ABCB1 was decreased by either T2R38 siRNA (small interfering RNA) or treatment with YM022, a gastrin receptor antagonist. Thus gut ABCB1 is regulated through signalling by CCK/gastrin released in response to PTC stimulation of T2R38 on enteroendocrine cells. We also show that PTC increases the efflux activity of ABCB1, suggesting that T2R signalling limits the absorption of bitter tasting/toxic substances through modulation of gut efflux membrane transporters.

scholarly journals Expression of the Bitter Taste Receptor, T2R38, in Enteroendocrine Cells of the Colonic Mucosa of Overweight/Obese vs. Lean Subjects

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0147468 ◽  
Author(s):  
Rocco Latorre ◽  
Jennifer Huynh ◽  
Maurizio Mazzoni ◽  
Arpana Gupta ◽  
Elena Bonora ◽  
...  
Keyword(s):  
Colonic Mucosa ◽  
Bitter Taste ◽  
Taste Receptor ◽  
Enteroendocrine Cells ◽  
Bitter Taste Receptor

scholarly journals PSVI-7 Variation in bitter taste receptor genes in three breeds of goats

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 206-206
Author(s):  
Mulumebet Worku ◽  
Kingsley Ekwemalor
Keyword(s):  
Bitter Taste ◽  
Taste Receptor ◽  
Capra Hircus ◽  
Gene Variants ◽  
Toxic Substances ◽  
Bitter Taste Receptor ◽  
Dietary Preference ◽  
Nucleotide Database ◽  
Boer Goats ◽  
Larger Sample

Abstract The objective of this study was to detect bitter taste receptor (T2Rs) variants in three breeds of goats. The ability to taste bitter taste impacts feed intake, digestion, and rejection of potentially toxic substances. Blood was collected from three breeds of goats (Spanish, Savannah, and Boer n = 5 /breed). Genomic DNA was extracted. The concentration and purity of DNA was determined using the Nanodrop spectrophotometer. Primers specific for seven T2R gene variants (T2R3, T2R4, T2R10, T2R12, T2R13, T2R16, and T2R67) were used to detect the goat T2R gene based on average threshold cycle. DNA products were commercially sequenced (Eurofins Genomics). The sequenced products were used in BLAST against the Capra hircus redundant nucleotide database. All seven taste gene variants were detected in the Savannah breed, In Spanish goats T2R4 and T213 were not detected, In Boer goats only T2R3, T2R16 and T2R13 were detected. Polymorphisms in T2R impact dietary preference, innate immunity and health. Thus, studies are needed to ascertain the possible functional significance of this variation using a larger sample size

Bitter Taste Receptor T2R138 in Mouse Enteroendocrine Cells is a Sensor for the Quorum Sensing Molecule, Acylhomoserine Lactone

2017 ◽  
Vol 152 (5) ◽  
pp. S823
Author(s):  
Jennifer Huynh ◽  
Filippo Caremoli ◽  
James Sinnett-Smith ◽  
Steven H. Young ◽  
Rocco Latorre ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Bitter Taste ◽  
Taste Receptor ◽  
Enteroendocrine Cells ◽  
Bitter Taste Receptor ◽  
Acylhomoserine Lactone ◽  
Quorum Sensing Molecule

par-4, a gene required for cytoplasmic localization and determination of specific cell types in Caenorhabditis elegans embryogenesis.

Genetics ◽  
1992 ◽  
Vol 130 (4) ◽  
pp. 771-790 ◽  
Author(s):  
D G Morton ◽  
J M Roos ◽  
K J Kemphues
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Types ◽  
Intestinal Cells ◽  
Specific Cell ◽  
Cytoplasmic Localization ◽  
Loss Of Function ◽  
Embryo Viability ◽  
Cell Stage ◽  
Maternal Genome

Abstract Specification of some cell fates in the early Caenorhabditis elegans embryo is mediated by cytoplasmic localization under control of the maternal genome. Using nine newly isolated mutations, and two existing mutations, we have analyzed the role of the maternally expressed gene par-4 in cytoplasmic localization. We recovered seven new par-4 alleles in screens for maternal effect lethal mutations that result in failure to differentiate intestinal cells. Two additional par-4 mutations were identified in noncomplementation screens using strains with a high frequency of transposon mobility. All 11 mutations cause defects early in development of embryos produced by homozygous mutant mothers. Analysis with a deficiency in the region indicates that it33 is a strong loss-of-function mutation. par-4(it33) terminal stage embryos contain many cells, but show no morphogenesis, and are lacking intestinal cells. Temperature shifts with the it57ts allele suggest that the critical period for both intestinal differentiation and embryo viability begins during oogenesis, about 1.5 hr before fertilization, and ends before the four-cell stage. We propose that the primary function of the par-4 gene is to act as part of a maternally encoded system for cytoplasmic localization in the first cell cycle, with par-4 playing a particularly important role in the determination of intestine. Analysis of a par-4; par-2 double mutant suggests that par-4 and par-2 gene products interact in this system.

scholarly journals A Cross-Sectional Study of Bitter-Taste Receptor Genotypes, Oral Health, and Markers of Oral Inflammation

Oral ◽  
2021 ◽  
Vol 1 (2) ◽  
pp. 122-138
Author(s):  
Kiranjit Kaur ◽  
Alexandria Turner ◽  
Patrice Jones ◽  
Dean Sculley ◽  
Martin Veysey ◽  
...  
Keyword(s):  
Oral Health ◽  
Bitter Taste ◽  
Taste Receptor ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Bitter Taste Receptor ◽  
Cross Sectional ◽  
Tnf Α ◽  
Oral Inflammation ◽  
Major Allele

(1) Background: The aetiology of oral disease is multifactorial, involving genetic and environmental factors, including dietary ones. Bitter taste genetics may be related to oral health through dietary modulation or non-gustatory roles, including modulation of inflammation. Investigations of bitter taste and oral health associations to date have been restricted to specific polymorphisms, limited outcomes (caries), and age-groups (children), and links to inflammation remain to be elucidated. (2) Methods: A cross-sectional study (n = 65) investigated the correlations between bitter taste genotypes, oral health outcomes, and oral inflammation markers. Oral examinations were conducted, including saliva testing with evaluation of flow rate, pH, and buffering and antioxidant capacity (FRAP) and IL-1β, TNF-α, IL-6 levels. DNA was collected via buccal swabs and used to evaluate the presence of multiple bitter-taste receptor gene polymorphisms. (3) Results: The major allele for TAS2R4-rs2233998, TAS2R5-rs2227264, TAS2R50-rs1376251, and TAS2R9-rs3741845 was associated with a higher mean of unstimulated salivary flow rate, FRAP, TNF-α, IL-1β, and likelihood of filled teeth. Presence of the major allele for TAS2R4-rs2234001 and TAS2R9-rs3741845 was associated with lower means FRAP, TNF-α, IL-1β, DMFT index, and likelihood of missing teeth. (4) Conclusions: These findings suggest relationships between bitter-taste genotypes, oral health outcomes, and inflammatory markers. These findings justify the need for further studies that could help identify risk groups and develop novel agents for maintaining oral health.

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