acesulfame potassium google scholar

It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide, This PDF is available to Subscribers Only. Thus, better understanding of the mechanisms underlying this variability may facilitate improved product formulation, with the potential to substantially impact health and wellness. In this study, we applied DNA sequencing and metabolomics approaches to characterize the gender-specific effects of Ace-K consumption on gut microbiota and their metabolism. Toxic products or endotoxins, such as LPS, generated by gut bacteria can enter systemic circulation and induce chronic inflammation [45–47]. D. Zuniga Additionally, the TAS2R31 alleles do not appear to influence sweetness, at least at the concentration tested here. B DNA samples were available from 147 participants. For analysis of individual SNPs, analysis of variance (ANOVA) was performed via proc mixed in SAS. Thus, a tag SNP approach is used here for TAS2R31, as the only published method for determining the Arg35Trp SNP, direct sequencing, is beyond the scope of the current project. MG Sullivan Ace-K consumption altered the gut bacterial composition and metabolism profile, and the perturbations were highly gender dependent. KK Contents. . Yes Below, we describe individual analyses for each SNP; however, these 3 SNPs are in LD, as shown in Figure 1 (bottom). G Howard The 1-kHz tones were generated with a Maico MA39 audiometer calibrated to deliver the specified sound pressure level binaurally; stimuli ranged from 50 to 90 dB in 10 dB steps. Fig 1B and 1C show the genera of gut bacteria that were significantly changed (p<0.05) in female and male mice. Odor and/or flavor descriptions from others (if found). 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]. JE Brockhoff Effect of the TAS2R9 Val187Ala polymorphism on the bitterness and sweetness of AceK and bitterness of PROP. This could be due to other factors like fungiform papillae density (Zuniga et al. Genes involved in carbohydrate transport (A), glycolysis and the TCA cycle (B), as well as carbohydrate degradation and fermentation (C), were consistently increased. BV LM G Similarly, a recent study found that Sutterella spp. As shown in Fig 4A and 4C, many genes involved in LPS synthesis were increased in mice after Ace-K consumption. Likewise, we did not measure food intake, body composition and relevant fat pads of mice, which represents another limitation of the study. They also note the rs3741845 SNP results in amino acid change in a region thought to alter the binding pocket of hT2R receptors (Dotson et al. VB 2020-10-24. GW . Smith However, no significantly increased body weight gain was observed in female mice. broad scope, and wide readership – a perfect fit for your research every time. Tag SNPs believed to be in complete LD with the putatively causal SNP in TAS2R31 predicted variation in AceK bitterness. 2000; Chandrashekar et al. JE 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]. Body weight was measured before and after the treatment. These data suggest that perturbation of the gut microbiome by Ace-K enriched the LPS synthesis-related genes, which might increase the risk of chronic inflammation in the host. . The fecal metabolomic profiling results suggested that Ace-K consumption can significantly change the gut metabolic profiles, which can influence the crosstalk between the host and gut microbiome. Møller Prospective participants were prescreened to ensure they qualified. The program Haploview (Barrett et al. 2007). JP Genes encoding LPS metabolism proteins (C) and thiol-activated cytolysin (D) were increased in Ace-K-treated male mice. NG Pyruvate is one of the key metabolites related to energy metabolism and can be further fermented to various SCFAs, such as propionate and butyrate [41]. Sigman-Grant Foreyt Bufe Shaw Barbarossa Taken together, these results may provide novel insights into understanding the functional interaction between artificial sweeteners and the gut microbiome and the role of this interaction in the development of obesity and chronic inflammation. However, based on our in vivo data, we would have expected Meyerhof’s team to identify AceK as a potential hT2R9 ligand in vitro. After leaving the laboratory, participants completed several personality questionnaires via web form. DM S Snyder (2011) found that when Ile240 was changed to Val240, this substitution had no effect on the activation of hT2R31 by AceK. Dotson Knopik here. Only AceK and PROP (see next section) data are reported here; data for the other stimuli will be reported elsewhere. 2010). Data presented here are part of a larger, ongoing study of the genetics of oral sensation (Project GIANT-CS). . 2005). There are 25 bitter taste receptor genes (TAS2Rs) in humans (Adler et al. Duffy Hayes TB. . We found no evidence that the Ala227Val SNP was associated with AceK sweetness [F(2,98) = 0.15; P = 0.86] or the perceived bitterness ratings of PROP [F(2,98) = 1.27; P = 0.29]. For permissions, please e-mail: journals.permissions@oup.com, Clinical Science in the Chemical Senses: Mechanisms, Perception, Behaviors, and Disorders, Enhanced odorant localization abilities in congenitally blind but not in late-blind individuals, The influence of cognitive parameters on olfactory assessment in healthy children and adolescents. Kim Bartoshuk J E Bartoshuk However, psychophysical data in humans do not always agree with in vitro expression study cells (compare Bufe et al. SM Roudnitzky et al. No, Is the Subject Area "Bacteroides" applicable to this article? Interestingly, cholic acid (CA) was increased, while deoxycholic acid (DCA) was dramatically decreased in the feces of male mice (Fig 6B). Haplotype pairs were assigned to each participant of European ancestry using PHASE (Stephens et al. In in vitro heterologous expression systems, site-directed mutation indicates that the amino acid at site 49 is the primary determinant of PROP response, with an additional influence arising from the residue at site 262; the residue at site 296 does not seem to matter, at least in cultured cells (Bufe et al. Supplementary material can be found at Supplementary Data. Overall intensity ratings for each stimulus were obtained with a gLMS. Li Adler Bacteroides is one of the most abundant and well-studied members of commensal microbiota. 2012). Bufe Herbstman Schiffman M The first SNP in this haplotype, Ala49Pro, is known to be in strong LD with the other 2 TAS2R38 SNPs, Val262Ala and Val296Ile (not measured here), such that more than 95% of individuals carry either the PAV or AVI variant (Kim et al. Duffy Finally, participants completed a standard propylthiouracil (PROP) phenotyping protocol with PROP, salt, and tones. An Agilent 6890/5973 GC-MS system equipped with a DB-5ms column (Agilent, Santa Clara, CA) was used to conduct the metabolomic profiling and capture all detectable metabolite features over a mass range from 50 to 600 m/z. 2004; Dinehart et al. 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). D. Green C Previously, Dotson and colleagues reported that saccharin did not activate hT2R9 in vitro; however, the top concentration used in their study was ~100 times lower than the amount required to elicit hT2R31 response in vitro (Pronin et al.

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