The underlying mechanisms of taste interactions in humans are not well understood, and three mechanisms have been proposed, namely a chemical interaction, a peripheral physiological, and a central mechanism. In the present study, it was investigated which of these mechanisms causes the suppression of sweetness by citric acid. This was investigated using a split-tongue gustometer that can stimulate the two sides of the tongue with different stimuli simultaneously, enabling a comparison of sucrose and citric acid presented either separately on each side of the tongue simultaneously or in a mixture on one side. Two studies were conducted using low (Study 1; n = 50) and high (Study 2: n = 59) concentrations of sucrose (2.5% (w/w) and 10% (w/w), respectively), and citric acid (0.14% (w/w) and 0.18% (w/w), respectively). In neither of the studies was there a significant difference in sweetness intensity ratings between the two conditions where sucrose and citric acid were presented either separately or in a mixture form. However, both showed significantly lower sweetness ratings than without citric acid indicating suppression of the sweetness of sucrose from citric acid. This provides strong evidence for a central mechanism for the suppression of the sweetness of sucrose by citric acid. This mechanism seems to be equal in high and low concentrations of both sucrose and citric acid.
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http://dx.doi.org/10.1093/chemse/bjad036 | DOI Listing |
Vet Med Sci
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Department of Reproduction and Artificial Insemination, Faculty of Veterinary Medicine, İstanbul University-Cerrahpasa, Avcilar, İstanbul, Turkey.
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Friedrich Alexander University Erlangen Nuremberg: Friedrich-Alexander-Universitat Erlangen-Nurnberg, Department of Materials Science, GERMANY.
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Plants for Human Health Institute, North Carolina State University, Kannapolis, NC, 28081, USA.
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Department of Ophthalmology, Tufts Medical Center, Tufts University School of Medicine, Boston, MA, 02111, USA.
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The Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA.
Alzheimer disease is a neurodegenerative pathology-modifying mitochondrial metabolism with energy impairments where the effects of biological sex and DNA repair deficiencies are unclear. We investigated the therapeutic potential of dietary ketosis alone or with supplemental nicotinamide riboside (NR) on hippocampal intermediary metabolism and mitochondrial bioenergetics in older male and female wild-type (Wt) and 3xTgAD-DNA polymerase-β-deficient (3xTg/POLβ) (AD) mice. DNA polymerase-β is a key enzyme in DNA base excision repair (BER) of oxidative damage that may also contribute to mitochondrial DNA repair.
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