Monell Chemical Senses Center

About: Monell Chemical Senses Center is a nonprofit organization based out in Philadelphia, Pennsylvania, United States. It is known for research contribution in the topics: Taste & Olfaction. The organization has 1173 authors who have published 2281 publications receiving 109542 citations. The organization is also known as: MCSC.

Prenatal and postnatal flavor learning by human infants.

Abstract: Background. Flavors from the mother9s diet during pregnancy are transmitted to amniotic fluid and swallowed by the fetus. Consequently, the types of food eaten by women during pregnancy and, hence, the flavor principles of their culture may be experienced by the infants before their first exposure to solid foods. Some of these same flavors will later be experienced by infants in breast milk, a liquid that, like amniotic fluid, comprises flavors that directly reflect the foods, spices, and beverages eaten by the mother. The present study tested the hypothesis that experience with a flavor in amniotic fluid or breast milk modifies the infants9 acceptance and enjoyment of similarly flavored foods at weaning. Methods. Pregnant women who planned on breastfeeding their infants were randomly assigned to 1 of 3 groups. The women consumed either 300 mL of carrot juice or water for 4 days per week for 3 consecutive weeks during the last trimester of pregnancy and then again during the first 2 months of lactation. The mothers in 1 group drank carrot juice during pregnancy and water during lactation; mothers in a second group drank water during pregnancy and carrot juice during lactation, whereas those in the control group drank water during both pregnancy and lactation. Approximately 4 weeks after the mothers began complementing their infants9 diet with cereal and before the infants had ever been fed foods or juices containing the flavor of carrots, the infants were videotaped as they fed, in counterbalanced order, cereal prepared with water during 1 test session and cereal prepared with carrot juice during another. Immediately after each session, the mothers rated their infants9 enjoyment of the food on a 9-point scale. Results. The results demonstrated that the infants who had exposure to the flavor of carrots in either amniotic fluid or breast milk behaved differently in response to that flavor in a food base than did nonexposed control infants. Specifically, previously exposed infants exhibited fewer negative facial expressions while feeding the carrot-flavored cereal compared with the plain cereal, whereas control infants whose mothers drank water during pregnancy and lactation exhibited no such difference. Moreover, those infants who were exposed to carrots prenatally were perceived by their mothers as enjoying the carrot-flavored cereal more compared with the plain cereal. Although these same tendencies were observed for the amount of cereal consumed and the length of the feeds, these findings were not statistically significant. Conclusions. Prenatal and early postnatal exposure to a flavor enhanced the infants9 enjoyment of that flavor in solid foods during weaning. These very early flavor experiences may provide the foundation for cultural and ethnic differences in cuisine.

Phytochemistry: ibuprofen-like activity in extra-virgin olive oil.

Abstract: Newly pressed extra-virgin olive oil contains oleocanthal--a compound whose pungency induces a strong stinging sensation in the throat, not unlike that caused by solutions of the non-steroidal anti-inflammatory drug ibuprofen. We show here that this similar perception seems to be an indicator of a shared pharmacological activity, with oleocanthal acting as a natural anti-inflammatory compound that has a potency and profile strikingly similar to that of ibuprofen. Although structurally dissimilar, both these molecules inhibit the same cyclooxygenase enzymes in the prostaglandin-biosynthesis pathway.

Evaluating the ‘Labeled Magnitude Scale’ for Measuring Sensations of Taste and Smell

Abstract: The Labeled Magnitude Scale (LMS) is a semantic scale of perceptual intensity characterized by a quasi-logarithmic spacing of its verbal labels. The LMS had previously been shown to yield psychophysical functions equivalent to magnitude estimation (ME) when gustatory, thermal and nociceptive stimuli were presented and rated together, and the upper bound of the LMS was defined as the 'strongest imaginable oral sensation'. The present study compared the LMS to ME within the more limited contexts of taste and smell. In Experiment 1, subjects used both methods to rate either taste intensity produced by sucrose and NaC1 or odor intensity produced by acetic acid and phenyl ethyl alcohol, with the upper bound of the LMS defined as either the 'strongest imaginable taste' or the 'strongest imaginable odor'. The LMS produced psychophysical functions equivalent to those produced by ME. In, Experiment 2 a new group of subjects used both methods to rate the intensity of three different taste qualities, with the upper bound of the LMS defined as the 'strongest imaginable [sweetness, saltiness, or bitterness]'. In all three cases the LMS produced steeper functions than did ME. Experiment 3 tested the hypothesis that the LMS yields data comparable to ME only when the perceptual domain under study includes painful sensations. This hypothesis was supported when the LMS again produced steeper functions that ME after subjects had been explicitly instructed to omit painful sensations (e.g. the 'burn' of hot peppers) from the concept of 'strongest imaginable taste'. We conclude that the LMS can be used to scale sensations of taste and smell when they are broadly defined, but that it should be modified for use in scaling specific taste (and probably odor) qualities. The implications of these results for theoretical issues related to ME, category-ratio scales and the size of the perceptual range in different sensory modalities are discussed.

Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.

Abstract: Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Because fructose, unlike glucose, does not stimulate insulin secretion, we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose. Blood samples were collected every 30-60 min for 24 h from 12 normal-weight women on 2 randomized days during which the subjects consumed three meals containing 55, 30, and 15% of total kilocalories as carbohydrate, fat, and protein, respectively, with 30% of kilocalories as either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high glucose (HGl)] beverage. Meals were isocaloric in the two treatments. Postprandial glycemic excursions were reduced by 66 +/- 12%, and insulin responses were 65 +/- 5% lower (both P < 0.001) during HFr consumption. The area under the curve for leptin during the first 12 h (-33 +/- 7%; P < 0.005), the entire 24 h (-21 +/- 8%; P < 0.02), and the diurnal amplitude (peak - nadir) (24 +/- 6%; P < 0.0025) were reduced on the HFr day compared with the HGl day. In addition, circulating levels of the orexigenic gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h after ingestion of each HGl meal (P < 0.01), but postprandial suppression of ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs. HGl). Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycerides compared with the HGl day (P < 0.005). Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose.

Intestinal epithelial tuft cells initiate type 2 mucosal immunity to helminth parasites

Abstract: Helminth parasitic infections are a major global health and social burden. The host defence against helminths such as Nippostrongylus brasiliensis is orchestrated by type 2 cell-mediated immunity. Induction of type 2 cytokines, including interleukins (IL) IL-4 and IL-13, induce goblet cell hyperplasia with mucus production, ultimately resulting in worm expulsion. However, the mechanisms underlying the initiation of type 2 responses remain incompletely understood. Here we show that tuft cells, a rare epithelial cell type in the steady-state intestinal epithelium, are responsible for initiating type 2 responses to parasites by a cytokine-mediated cellular relay. Tuft cells have a Th2-related gene expression signature and we demonstrate that they undergo a rapid and extensive IL-4Rα-dependent amplification following infection with helminth parasites, owing to direct differentiation of epithelial crypt progenitor cells. We find that the Pou2f3 gene is essential for tuft cell specification. Pou2f3(-/-) mice lack intestinal tuft cells and have defective mucosal type 2 responses to helminth infection; goblet cell hyperplasia is abrogated and worm expulsion is compromised. Notably, IL-4Rα signalling is sufficient to induce expansion of the tuft cell lineage, and ectopic stimulation of this signalling cascade obviates the need for tuft cells in the epithelial cell remodelling of the intestine. Moreover, tuft cells secrete IL-25, thereby regulating type 2 immune responses. Our data reveal a novel function of intestinal epithelial tuft cells and demonstrate a cellular relay required for initiating mucosal type 2 immunity to helminth infection.