125 Poster <strong>Chemosensory</strong> Coding and ClinicalCAN HETEROSEXUAL MEN AND WOMEN DISCRIMINATEEACH OTHER FROM THEIR AXILLARY SECRETIONS? IFSO, DO THEY EXHIBIT A PREFERENCE?Reynolds D.J. 1 , Fisher R.J. 2 , Scott L. 1 , Kemp S. 3 1 Univ. of Chester,Chester, United Kingdom; 2 Consumer Science, Unilever R&D, Wirral,United Kingdom; 3 Unilever R&D, Bedfordshire, United KingdomHeterosexual participants (16 male; 24 female) identified the genderof an axillary sample (Study 1) and selected their preferred sample(Study 2) in a 2AFC task. Each study consisted of 25 intensity-matchedpairs (male and female samples). Prior to the study, fabric swatcheswere worn in the under-arm for a 24-hour period by 89 volunteers (40male; 49 female). Samples were coded and double-blind rated by 8odour assessors trained and experienced in evaluating axillary intensity.For Study 1 planned one sample t-tests (2-tail) were performed on meanaccuracy for each gender separately, revealing that males (57.3%accuracy) and females (55.2%) identified the gender of samplesignificantly above chance. Study 2 (preference) revealed that femalessignificantly preferred the swatches from female derived samples(56.7%). In contrast, males showed no preference for male or femalederived samples. Results from the gender identification study challengeobservations of near-universal superiority of females in olfactoryfunction (Koelega, 1994; Doty, 1991) and suggest that males can beequally sensitive to biologically relevant odours. The preference studybuilds on findings by Martins, Preti, Crabtree and Wysocki (2005) whorevealed patterns of preference that differed across groups ofindividuals having different sexual orientations. Our results now show asignificant heterosexual female preference for heterosexual femaleodours. Although contradicting a sexual orientation based explanationhormonal fluctuations during the menstrual cycle, familiarity with owngenderrelevant odours, and mate search during the ovulatory periodonly may offer alternative interpretations of these results.126 Poster <strong>Chemosensory</strong> Coding and ClinicalWITHDRAWN127 Poster <strong>Chemosensory</strong> Coding and ClinicalLEPTIN, INSULIN AND SWEET TASTE IN GESTATIONALDIABETES MELLITUSBelzer L. 1 , Tepper B.J. 1 , Ranzini A. 2 , Smulian J. 3 1 Food Science,Rutgers University, New Brunswick, NJ; 2 Maternal & Fetal Medicine,St. Peter's University Hospital, New Brunswick, NJ; 3 UMDNJ-RobertWood Johnson Medical School, New Brunswick, NJLeptin is the protein product of the LEP gene and is associated withadiposity, satiety and regulation of energy intake. The db/db mouse, agenetic model of diabetes that is hyperleptinemic but lacking afunctional leptin receptor, shows elevated behavioral responses to sweettaste (Ninomiya et al. 2002). Thus, leptin may exert effects on tastecells to modulate sweet taste. This relationship has not been studied indiabetic humans. This study assessed relationships between plasmaleptin and insulin, and sweet taste in women with gestational diabetesmellitus (GDM). We measured fasting plasma leptin and insulin in 12women with GDM at 24-28 wks gestation (at diagnosis), 68 pregnantwomen without GDM and 12 non-pregnant controls. Subjects also ratedsweetness intensity and liking of glucose solutions (0.01-0.16M) andcommercial fruit cocktail, using a 15-cm line scale. There were nogroup differences in sweetness intensity or liking for any of the stimuli.In women with GDM, leptin was correlated with sweetness intensity offruit cocktail (r = 0.58, p = 0.05) and insulin was correlated withsweetness liking of both the fruit cocktail (r = 0.61; p = 0.03) and theglucose solutions (averaged across concentrations) (r = 0.65, p = 0.02).These associations were not observed in the other study groups. Thesepreliminary findings are novel and suggest that leptin and insulin play arole in sweet taste disruptions in diabetic humans. Supported by NIHDC04702.128 Poster <strong>Chemosensory</strong> Coding and ClinicalREVISITING THE SWEET TOOTH: RELATIONSHIPSBETWEEN SWEETNESS PERCEPTION, SWEET FOODPREFERENCE, AND BMISnyder D.J. 1 , Duffy V.B. 2 , Moskowitz H. 3 , Hayes J.E. 2 , Bartoshuk L.M. 41 Surgery, Yale University, New Haven, CT; 2 Dietetics, University ofConnecticut, Storrs, CT; 3 Moskowitz-Jabobs, Inc., White Plains, NY;4 Center for Smell and Taste, University of Florida, Gainesville, FLAs Pangborn noted in 1958, an obese individual is commonly thoughtto have a sweet tooth, but an experiment in her lab with sweet foodsfailed to show any association between sweet liking and body size. Avariety of studies followed supporting the same conclusion. In addition,sensory studies suggest that perceived sweetness does not change withbody mass index (BMI). We have argued that across-group scalingcomparisons (e.g., obese vs. non-obese) are invalid unless investigatorsshow that scale labels denote the same experiences to all. We solve thisdilemma by asking subjects to rate sensory and hedonic experiences inlarger contexts (i.e., all sensation, all hedonic experience). Datacollected in this manner produced conclusions that differ from priorfindings. In particular, sucrose liking (measured with the hedonicgLMS) rises with rising BMI, but the perceived sweetness of a candy(measured with the gLMS) declines. Thus, to make valid comparisonsof sweet liking across BMI, sweet liking must be corrected for variationin perceived sweetness with BMI. Following Moskowitz´s lead, wecompared sucrose sweetness/liking functions for underweight, normal,overweight, and obese individuals. As BMI increases, the slope of thefunction increases; that is, for the same perceived sweetness, sweetliking increases with BMI. Funding: NIDCD 00028332
129 Poster <strong>Chemosensory</strong> Coding and ClinicalPROP BITTERNESS AND CARDIOVASCULAR DISEASE(CVD) RISK FACTORS IN ADULT WOMENDuffy V.B. 1 , Fernandez M.L. 2 , Lanier S. 1 , Aggarwal D. 2 , Bartoshuk L. 31 Dietetics, Univ. of Connecticut, Storrs, CT; 2 Nutritional Sciences, Univ.of Connecticut, Storrs, CT; 3 Yale University, New Haven, CTPrevious research from our group has found relationships betweenmeasures of taste genetics and CVD risk factors in middle-aged men,elderly women, and preliminary findings among middle-age women.Here we examined this relationship in 86 females (mean age=45±9 yrs)with multivariate analysis, controlling for non-taste factors that affectCVD risk (p ≤ 0.05). Using the general labeled magnitude scale, Ssrated the bitterness of 6-n-propylthiouracil (PROP) and preference forsurveyed high fat foods as well as reported frequency of consumingcore high-fat foods on a validated instrument. For CVD risk assessment,total cholesterol, HDL and LDL subfractions were analyzed fromfasting venous bloods and adiposity calculated from measuredheight/weight and waist circumferences. Resting blood pressure wasmeasured on women who were 35 years and older (n = 75). Those whotasted less bitterness from 3.2 mM PROP averaged greater preferenceacross 14 high-fat foods and more frequent intake of a 40-item high-fatgroup. As reported previously, PROP bitterness was negativelycorrelated with central adiposity, but only in those without excessiveobesity (circumference≤40 inches; n = 76). Those tasting less PROPbitterness showed greater CVD risk factors—higher systolic bloodpressures, higher LDL and lower HDL cholesterol subfractions. Thesedata support that those who taste PROP as least bitter may have greatestCVD risk and that the relationship may be mediated in part throughdietary behaviors toward high-fat foods. (NRICGP/USDA funded)130 Poster <strong>Chemosensory</strong> Coding and ClinicalINFLAMMATORY PATHWAYS MAY UNDERLIE EARLYTASTE LOSS AND TASTE CELL DEATH CAUSED BYRADIATION THERAPYNelson G. 1 , Cao J. 2 , Gillespie Y. 3 , Brand J. 4 1 Neurobiology, Univ ofAlabama, Birmingham, Birmingham, AL; 2 Monell Chemical SensesCenter, Philadelphia, PA; 3 Comprehensive Cancer Center, Univ ofAlabama, Birmingham, Birmingham, AL; 4 Univ of Pennsylvania &Monell Chemical Senses Center, Philadelphia, PATaste loss is a distressing side effect experienced by nearly all cancerpatients who receive head and neck radiation therapy. There is notreatment. Single dose and fractionated radiation rat and mouse modelssuggest that inflammation may play a role in the development of earlytaste loss and ultimately mediate taste cell death. We propose that theradiation-induced inflammation is mediated primarily via NFkBpathways, leading to cell death via oncosis/autophagy programmed celldeath. Preliminary histological findings at early post-radiation timepoints only show the presence of a marked inflammatory infiltrate.Using rt-PCR, following a single 18 Gy dose at 4 days survival, there isan increase in IL-6 in rat fungiform and Bax and ICAM-1 in posteriortaste tissue. Following two fractions of 5 Gy in mice, taste tissues showchanges in expression levels of certain chemokines, cytokines and otherfactors involved in an inflammatory response including, for example,Il12b, Il1r1, Fcer1g, Fcgr1, Scye1 , Ccl8, Cxc10, IL1r2, IL5, integrin,and TLr9. Most of these factors are players in inflammatory pathwaysmediated by NFkB. Immunohistochemistry results demonstrate that theapoptotic indicators TUNNEL and caspase 3 are not elevated at 2 or 25days following radiation. Electron micrographs of rat taste cells 7 daysafter a single 18 Gy dose show even margination of chromatin,degenerating membranes, and cytosolic double membrane vesicles,features of oncosis/autophagy programmed cell death. These datasuggest that early activation of inflammatory pathways, perhapsmediated by NFkB, may represent the mechanism underlying earlyradiation taste loss and subsequent taste cell death.131 Poster <strong>Chemosensory</strong> Coding and ClinicalPHENYLTHIOCARBAMIDE (PTC) PERCEPTION INPATIENTS WITH SCHIZOPHRENIA AND FIRST-DEGREEFAMILY MEMBERSMoberg P.J. 1 , McGue C. 1 , Kanes S. 1 , Roalf D. 1 , Balderston C. 1 , Gur R. 1 ,Turetsky B. 1 1 University of Pennsylvania, Philadelphia, PAThe inability to taste phenylthiocarbamide (PTC) has been associatedwith a number of medical and neurological illnesses not typicallyrelated to taste. We examined PTC sensitivity in schizophrenia patientsand non-ill first degree relatives to determine whether taster status couldrepresent a simple vulnerability marker. Method: PTC sensitivity wasassessed in 67 schizophrenia patients, 30 healthy-comparison subjectsand 31 first-degree family members. Results: A higher incidence ofnontasters was seen in patients and family members relative to healthycomparison subjects. Among patients, analysis of clinical symptomratings revealed that non-tasting patients exhibited increased levels ofnegative and first-rank symptoms, characteristic of those seen in thedeficit syndrome. In addition, non-tasting patients also showed poorerodor identification skills relative to those patients who could taste PTC.These differences were not explained by sex, age, or cognitiveimpairment. Conclusions: These data demonstrate a higher incidence ofnontasters to PTC in patients with schizophrenia and non-ill first degreefamily members. Phenotypic variation in PTC sensitivity is thought tobe genetic in origin and may suggest a somewhat higher risk for illnessin those subjects with the recessive alleles. Funded in part by NationalInstitutes of Health Grant MH-63381and an Independent InvestigatorAward from the National Alliance for Research on Schizophrenia andDepression132 Poster <strong>Chemosensory</strong> Coding and ClinicalRETRONASAL OLFACTION AND OTITIS MEDIACollins S.P. 1 , Snyder D.J. 2 , Catalanotto F.A. 3 , Bartoshuk L.M. 31 Otolaryngology Department, University of Florida, Gainesville, FL;2 Neuroscience, Yale University, New Haven, CT; 3 Center for Smell andTaste, University of Florida, Gainesville, FLRetronasal olfaction is perceptually localized in the mouth eventhough odorants are actually stimulating receptors at the olfactorymucosa. Taste plays a role in that localization. Taste also contributes tothe perceived intensity of retronasal olfaction for congruenttaste/odorant pairs. For example, adding sugar will intensify thesensation of pear from pear juice, adding salt will not. We reasoned thatif increasing taste intensity could increase retronasal olfactory intensity,then decreasing taste intensity might decrease retronasal olfactoryintensity. At AChemS 2005 we showed data consistent with that idea;nontasters of PROP (who perceive reduced taste intensities) perceivedless retronasal olfaction for the same perceived intensity of orthonasalolfaction. Here we demonstrate another finding consistent with thetaste/retronasal connection. Otitis media (OM) can damage taste sincethe chorda tympani taste nerve passes through the middle ear on its wayto the brain. Does this taste damage result in reduced retronasalolfaction? Attendees at lectures sniffed a strawberry candy (orthonasalolfaction) and rated the strawberry sensation on the gLMS. They thenchewed and swallowed the candy and rated the strawberry sensation(retronasal olfaction) again. Comparing regression plots of retronasalstrawberry intensity as a function of orthonasal strawberry intensity forthose with no histories of OM and those with histories of moderate tosevere OM showed significantly lower slopes for the OM subjects. Thatis, for the same orthonasal intensity, the OM subjects perceived lessretronasal intensity. This has implications for the way in which sensoryalterations alter food preferences and thus lead to weight increases.Funding: NIDCD 000283.33
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