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PubMed1979

Bitter-sweet success.

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Drug and Narcotic Control↗
PubMed1978

Bitter medicine.

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Economics, Hospital↗
PubMed1978

Four new methods of debittering protein hydrolysates and a fraction of hydrolysates with high content of essential amino acids.

Extraction of enzymatic protein hydrolysates with azeotropic secondary butyl alcohol (SBA) or aqueous ethanol (AE) or aqueous isopropranol (AI), seems to be an efficient and generally applicable method for removal of bitter compounds. The bitter peptides are concentrated in the alcohol-phase which has an extremely bitter taste. It has a concentration of 40-70 p. 100 essential amino-acids. In the alcohol-phase leucine, isoleucine, phenylalamine and tryptophan were particularly increased. Experiments showed that the bitterness of the alcohol-soluble fraction could be reduced by applying the plastein reaction. A reduction in bitterness of protein hydrolysates could also be achieved by applying hydrophobic interaction chromatography. Of tested gels, hexyl-sepharose was found to be the most effective for debittering of protein hydrolysates.

Amino Acids↗
PubMed1977

Enzymatic oxydation of linoleic acid: formation of bittertasting fatty acids.

Linoleic acid was oxidized with a protein fraction from soya beans (25 degrees C; 2h), in which lipoxygenase and peroxydase activities occurred. The fatty acids formed were isolated and, after emulsification with a sugar ester, were evaluated for bitter taste. The main components of the bitter-tasting fractions was a mixture of 9.12.13-trihydroxyoctadec-10- and 9.10.13-trihydroxyoctadec-11-enoic acids. The taste threshold lies in the range 0.6-0.9 mumol/ml. Two further trihydroxy-acids and two oxodihydroxy-acids were also identified in the bitter-tasting fraction.

Fatty Acids↗
PubMed1977

[Investigation about the taste of di, tri- and tetrahydroxy fatty acid].

Two diastereomeric 9, 10-dihydroxystearic acids, four diasteromeric 9,10,12-trishydroxystearic acids, a mixture of diastereomeric 9,10,12,13-tetrahydroxystearic acids, a mixture of 9.12,13,-trihydroxy-10 trans- and 9,10,13-trihydroxy-11-trans-octadecenoic acids (tri-OH-mixture from lipoxygenase catalysis) and the hydrogenated tri-OH mixture were tested for bitter taste. Only the tri - and tetrahydroxy acids are bitter. The taste thresholds of the saturated tri- and tetrahydroxy acids are in the range from 1.0--4.3 micron ol/ml. There are no significant differences in the taste thresholds between the four diastereomeric 9,- 10,12-trihydroxy acids. The double bond in the trihydroxy acids from the lipoxygenase catalysis enhances the bitter taste 3-fold.

Humans↗
PubMed1979

Evidence for neural inhibition in bittersweet taste mixtures.

Three lines of evidence from psychophysical experiments implied that mutual suppression of bitter and sweet tastes is due to neural inhibition rather than chemical interactions in solution or competition of molecules for common receptor sites. Removal of sweetness from bittersweet mixtures caused the bitterness to increase. This was accomplished by adaptation to sucrose or by treatment with Gymnema sylvestre, neither of which affect the concentration of sucrose on the tongue. Such increases in the bitterness of mixtures, independent of the concentration of the sweet masking substance, are difficult to reconcile with suppression by means of chemical interactions. Similar dependence of suppression on perceived intensity (and independence from concentration) was observed with mixtures of phyenylthiocarbamide and sucrose. Tasters of phenylthiocarbamide showed stronger suppression of sweetness than nontasters. This result was also inconsistent with molecular interactions causing suppression, which would have resulted in the same degree of suppression for the two groups. Instead, these findings support neural explanations of mixture suppression, such as antidromic inhibition or occlusion.

Adaptation, Physiological↗
PubMed2026

CgMYC2 directly activates jasmonate-induced naringin biosynthesis in Citrus grandis 'Tomentosa'.

CgMYC2 links jasmonate signaling to naringin biosynthesis by binding G-box motifs and activating flavonoid-pathway promoters in Citrus grandis 'Tomentosa' Naringin, the predominant bitter-flavanone glycoside in Citrus grandis 'Tomentosa', has well-characterized biosynthetic enzymes, yet the transcriptional regulators coupling hormonal signals to pathway activation remain poorly understood. We demonstrate that CgMYC2, a jasmonate-responsive bHLH transcription factor, functions as a central activator of naringin biosynthesis. Exogenous methyl jasmonate (MeJA) treatment increased naringin content 3.45-fold in seedlings, coinciding with a rapid 6.6-fold induction of CgMYC2 that preceded the peak transcription of five core biosynthetic genes (CgPAL5, CgCHS, CgFNS, Cg7GlcT, and Cg1,2RhaT). Physical interaction between CgMYC2 and the JAZ protein CgJAZ3 was confirmed by pull-down and Co-IP assays, placing CgMYC2 within the canonical jasmonate signaling cascade. Y1H confirmed CgMYC2 binding to the Cg1,2RhaT promoter, EMSA demonstrated direct G-box-dependent binding to all five pathway promoters, and dual-luciferase assays showed transactivation of all five promoters, with the strongest activation for CgCHS. As complementary chromatin-level support, a single-sample CUT&Tag profile revealed G-box-enriched CgMYC2-associated chromatin regions across jasmonate-responsive and secondary-metabolic loci. Virus-induced gene silencing (VIGS) of CgMYC2 reduced naringin content by ~21% and suppressed biosynthetic gene expression, supporting its positive contribution. Furthermore, heterologous overexpression in tomato activated the flavonoid pathway and elevated 16 flavonoid compounds, consistent with evolutionary conservation of the MYC2-G-box regulatory logic. These findings establish CgMYC2 as a central, JA-responsive activator bridging jasmonate perception and naringin biosynthesis, providing a molecular framework for the targeted improvement of bitter-flavonoid traits in citrus.

Citrus↗
PubMed1978

Effects of oral pH on cigarette smoking.

Permeability of nicotine across the oral mucosa had been shown to be a direct linear function of alkalinity in the oral cavity. Here, oral pH in cigarette smokers was manipulated from pH 5 to 8 by rinses with Sorenson's and McIlvaine's buffers. As a alkalinity increased, cigarette taste was perceived as stronger, more bitter, and, in some cases, more upleasant; and heart-rate accelerated slightly. Nicotine self-administration and blood pressure were not influenced. Differential absorption of nicotine and cross-adaptation of sour to bitter taste are both discussed as explanations for the results.

Blood Pressure↗
PubMed1978

Pituitary-adrenal axis and oral morphine consumption in rats.

Removal of the pituitary gland in rats leads to suppression of oral morphine and quinine intake behavior. Experiments measuring oral intake of solutions containing graded concentrations of morphine or quinine, revealed that the detection acuity for bitter taste is changed in hypophysectomized (hypox) animals. Treatment of these rats with ACTH 1--24 restored oral morphine intake towards that on intact rats. Morphine consumption in hypox rats was not affected by administration of ACTH 4--10 or ACTH 11--24, but was normalized by treatment with corticosterone. Adrenalectomy also diminished oral morphine intake. It is concluded that hypophysectomized animals refuse a morphine solution because their threshold for bitter taste quality is altered, presumably due to a diminished release of corticosteroids.

Adrenalectomy↗
PubMed2026

Predicting food taste with bound-driven optimization.

The prediction of sensory attributes from ingredient-level formulations is an emerging challenge at the intersection of food science and artificial intelligence. We address the fundamental question of whether the taste of a food can be predicted from its ingredients by treating recipes as composite materials. We apply Hashin-Shtrikman (HS) and Reuss-Voigt (RV) bounds, techniques originally developed for elastic moduli, as a null-hypothesis additive baseline for five taste dimensions (sweetness, sourness, bitterness, umami, saltiness) on a curated dataset of 70 recipes decomposed into 115 distinct ingredients scored against a library of 209 ingredient-level taste references with trained-panel ground truth. This baseline systematically under-predicts perceived taste: 77% of actual taste values exceeded the HS upper bound, with the exceedance rate ranging from 26% (bitterness) to 97% (saltiness). We traced this gap to specific processing chemistry (Maillard reactions, caramelization, evaporative concentration, protein hydrolysis, and nucleotide synergy) and introduced a hybrid model that augments the HS baseline with eight chemistry-proxy features encoding these mechanisms. Our results show that our interpretable hybrid model eliminates the systematic bias and reduces mean absolute error by 27%-62% for sweetness, sourness, umami, and saltiness while using only 10 interpretable features, achieving performance comparable to a black-box Lasso regression on 115 per-ingredient features. We further demonstrate constrained inverse design via Differential Evolution, recovering ingredient formulations that match target taste profiles subject to compositional bounds. Our work demonstrates how key chemical processes during food preparation can inform and augment physics-based and machine learning models, providing a quantitative fingerprint of processing chemistry's contribution to taste perception and paving the way for model-driven food formulation with targeted sensory characteristics.

Composite material bounds↗
PubMed2026

Genetics of sensory nutrition.

Sensory nutrition is an emerging research area that examines how chemosensory perception, particularly taste and smell, shapes dietary behaviours, nutritional status, and disease risk. Variation in how individuals perceive the same foods may help explain differences in diet quality and responsiveness to behavioural dietary interventions, yet chemosensory phenotypes are rarely measured at the population level. Genetic variation contributes to this perceptual diversity and provides a framework for investigating sensory determinants of diet using genomic approaches. This review summarises evidence linking chemosensory genetics to perception and dietary behaviours, and discusses applications for causal inference and for precision and personalised nutrition. Twin studies reveal moderate to high heritability for bitter taste traits, with more modest and phenotype-dependent estimates for sweetness, sourness, saltiness, fat-related traits, and olfactory measures. Genome-wide association studies have identified loci in taste and olfactory receptor genes associated with specific chemosensory traits as well as liking and intake of various foods, although the evidence remains concentrated on bitter taste and populations of European ancestry. These genetic variants have been used in Mendelian randomisation, a genetics-based approach that strengthens causal inference, to test whether sensory traits influence dietary behaviour. For precision nutrition, evidence for taste genotype-stratified interventions remains limited and mixed. Realising the promise of sensory nutrition will require scalable and standardised chemosensory phenotyping, Findable, Accessible, Interoperable, and Reusable (FAIR) data infrastructure, expanded research in diverse populations, and integration with broader biological and sociocultural determinants of dietary intake.

Genetics↗