Using polymorphisms found in TAS2Rs, which were previously shown to be functional for AceK and other nonnutritive sweeteners (i.e., saccharin) in vitro (Kuhn et al.
. 6-Methyl-1,2,3-oxathiazin-4(3H)-one 2,2-dioxide potassium salt. However, present data also suggest additional polymorphisms may contribute to the inability to perceive AceK bitterness. Egan
Using suprathreshold psychophysics in humans, we explained variation in the perceived intensity of AceK bitterness using a candidate SNP approach across multiple TAS2R genes. Therefore, we further investigated the functional gene alterations induced by Ace-K consumption. Effect of the TAS2R9 Val187Ala polymorphism on the bitterness and sweetness of AceK and bitterness of PROP. LD plot for TAS2R SNPs on chromosomes 7 (top) and 12 (bottom). Fry
In this study, we found that CA and DCA increased and decreased, respectively, after Ace-K treatment (Fig 6B), highlighting the effects of Ace-K on the homeostasis and biotransformation of bile acids, important signaling molecules in inflammation and glucose metabolism [54–57]. Conversely, putatively functional SNPs in TAS2R4, TAS2R38, and near TAS2R16 did not predict bitterness.
In particular, the interaction between the host and gut microbiome is complicated, and many host characteristics can influence the responses of the gut microbiome to external stimuli. The gut microbiome is deeply involved in host metabolism and plays a crucial role in food digestion and energy homeostasis in the human body [7–9]. B
There was no evidence that the rs1308724 SNP near TAS2R16 was a significant predictor of AceK bitterness [F(2,98)= 0.16; P = 0.85]. For example, common alleles for the genes TAS2R9 and TAS2R38 explain variable response to the bitter drugs ofloxacin in vitro and propylthiouracil in vivo.
2008), aspartame (Duffy et al.
Google Scholar: with word "flavor" Search: Google Scholar: with word "odor" Search: Perfumer and Flavorist: Search: Google Patents: Search: US Patents: Search: EU Patents: Search . There was little to no evidence that the bitterness of AceK varied with rs2234001 in TAS2R4 [F(2,97)= 0.69; P = 0.50]. 2004; Dinehart et al. Google Scholar; Soffritti M, Belpoggi F, Degli Esposti D, Lambertini L, Tibaldi E, Rigano A. Ace-K consumption led to a significant increase in body weight in male mice, potentially by disrupting the gut bacterial compositions and activating bacterial energy harvesting pathways.
In addition, the abundances of multiple genes involved in carbohydrate metabolism and fermentation pathways were also consistently increased (Fig 3C).
Acesulfame potassium and saccharin are well-studied nonnutritive sweeteners commonly found in food products. 2000; Chandrashekar et al. In this study, we investigated the effects of Ace-K on the gut microbiome and the changes in the fecal metabolome using 16S rRNA sequencing and gas chromatography-mass spectrometry (GC-MS) metabolomics. Likewise, we did not measure food intake, body composition and relevant fat pads of mice, which represents another limitation of the study.
The authors declare no other relationships or activities that may have influenced the work described here. In addition, multiple genes encoding flagella components, including flagella basal body P-ring formation protein FlgA, flagellar L-ring protein precursor FlgH, flagellar P-ring protein precursor FlgI and flagellar FliL protein, were increased, as shown in Fig 4B. 2002).
The concentrations were selected to produce a sensation near “moderate” on a gLMS for the main perceptual quality of the stimulus. The sweetness of AceK did not significantly differ across Gln217Glu [F(2,102) = 1.41; P = 0.25] nor was this SNP associated with the reported bitterness ratings of PROP [F(2,102) = 0.08; P = 0.93].
Recently, this finding was confirmed for the TAS2R38 genotype and A. bunius berries, although the specific ligand itself was not isolated (Reed D, personal communication). VB
Conversely, the bitterness of PROP was positively associated with AceK sweetness, predicting 10.2% of the variation (P < 0.001).