A cross-talk between fat and bitter taste modalities.

The choice of food is governed largely by the sense of taste. To date, five basic taste modalities have been described; however, there is an increasing agreement on the existence of a 6th fat taste. The taste modalities might interact with each other and also with other senses. The advancements in cellular and molecular biology have helped the characterization of taste signaling mechanisms, down to the receptor level and beyond. CD36 and GPR120 have been shown to be involved in the detection of fat taste while bitter taste is perceived by a number of receptors that belong to a family of taste-type 2 receptors (T2R or TAS2R). Hence, the most common role is played by TAS2R16 and TAS2R38 in bitter taste perception in humans. Increasing evidences from behavioural studies suggest that fat and bitter taste modalities might interact with each other, and this interaction might be critical in obesity. In the current review, we will discuss the evidence from genetic and behavioural studies and propose the molecular mechanism of a cross-talk between fat and bitter tastes.

Khan AS ，Murtaza B ，Hichami A ，Khan NA ... -  《-》

Taste perception and its effects on oral nutritional supplements in younger life phases.

Khan AS ，Hichami A ，Khan NA 《-》

Orosensory detection of bitter in fat-taster healthy and obese participants: Genetic polymorphism of CD36 and TAS2R38.

We assessed orosensory detection of a long-chain fatty acid, linoleic acid (LA), and a bitter taste marker, 6-n-propylthiouracil (PROP), and correlated lipid-taster subjects with PROP detection and polymorphism in genes encoding bitter and lipid taste receptors, respectively, TAS2R38 and CD36, in normal weight and obese subjects. The normal weight (n = 52, age = 35.3 ± 4.10 years, BMI = 23.22 ± 1.44 kg/m2) and obese (n = 52, age = 35.0 ± 5.43 years, BMI = 34.29 ± 5.31 kg/m2) participants were recruited to determine fat and bitter detection thresholds. The genomic DNA was used to determine single nucleotide polymorphism (SNP) of CD36 (rs1761667) and TAS2R38 (rs1726866 and rs10246939). The study included the participants who could detect LA, i.e., lipid-tasters. There was a positive correlation between BMI and detection thresholds for fat and bitter taste in normal weight and obese subjects. Obese participants showed a positive correlation between LA and PROP detection thresholds. PROP detection thresholds were higher for CD36 SNP (rs1761667) and TAS2R38 SNPs (rs1726866 and rs10246939) in obese participants compared to normal weight subjects. LA detection thresholds were not high for CD36 SNP (rs1761667) or TAS2R38 SNP (rs1726866 and rs10246939) in obese participants. Orosensory detection thresholds for fat and bitter taste are associated with BMI, and CD36 and TAS2R38 genotypes are not always associated with taste phenotypes.

Karmous I ，Plesník J ，Khan AS ，Šerý O ，Abid A ，Mankai A ，Aouidet A ，Khan NA ... -  《-》

CD36- and GPR120-mediated Ca²⁺ signaling in human taste bud cells mediates differential responses to fatty acids and is altered in obese mice.

It is important to increase our understanding of gustatory detection of dietary fat and its contribution to fat preference. We studied the roles of the fat taste receptors CD36 and GPR120 and their interactions via Ca(2+) signaling in fungiform taste bud cells (TBC). We measured Ca(2+) signaling in human TBC, transfected with small interfering RNAs against messenger RNAs encoding CD36 and GPR120 (or control small interfering RNAs). We also studied Ca(2+) signaling in TBC from CD36(-/-) mice and from wild-type lean and obese mice. Additional studies were conducted with mouse enteroendocrine cell line STC-1 that express GPR120 and stably transfected with human CD36. We measured release of serotonin and glucagon-like peptide-1 from human and mice TBC in response to CD36 and GPR120 activation. High concentrations of linoleic acid induced Ca(2+) signaling via CD36 and GPR120 in human and mice TBC, as well as in STC-1 cells, and low concentrations induced Ca(2+) signaling via only CD36. Incubation of human and mice fungiform TBC with lineoleic acid down-regulated CD36 and up-regulated GPR120 in membrane lipid rafts. Obese mice had decreased spontaneous preference for fat. Fungiform TBC from obese mice had reduced Ca(2+) and serotonin responses, but increased release of glucagon-like peptide-1, along with reduced levels of CD36 and increased levels of GPR120 in lipid rafts. CD36 and GPR120 have nonoverlapping roles in TBC signaling during orogustatory perception of dietary lipids; these are differentially regulated by obesity.

Ozdener MH ，Subramaniam S ，Sundaresan S ，Sery O ，Hashimoto T ，Asakawa Y ，Besnard P ，Abumrad NA ，Khan NA ... -  《-》

Genetic influences on oral fat perception and preference: Presented at the symposium "The Taste for Fat: New Discoveries on the Role of Fat in Sensory Perception, Metabolism, Sensory Pleasure and Beyond" held at the Institute of Food Technologists 2011 An

Research suggests that dietary fat is perceived not only by texture, but also by taste. However, the receptors for chemosensory response to fat have not been identified. We report on 2 genes,TAS2R38 and CD36, that may play a role in fat perception and preference in humans. TAS2R38 is a taste receptor for bitter thiourea compounds, including 6-n-propylthiouracil (PROP) and phenylthiocarbamide (PTC). Nontasters of these compounds tend to be poor at discriminating fat in foods, even though they prefer higher fat versions of these foods. CD36, a fatty acid translocase expressed on multiple cell types including taste cells, plays a critical role in fat preferences in animals. In studies conducted in our laboratory with African-American adults, we identified a variant in the CD36 gene, rs1761667, that predicts oral responses to fat. Individuals who have the A/A genotype at this site tend to find Italian salad dressings creamier than those who have other genotypes at this site. In addition, A/A individuals report higher preferences for added fats, oils, and spreads (for example margarine). Assuming these data are confirmed in other populations, screening for CD36 genotype may provide helpful information to food companies for developing fat-modified products.

Keller KL 《-》