Oral sensitivity to fatty acids, food consumption and BMI in human subjects
Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty aci...
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Published in | British journal of nutrition Vol. 104; no. 1; pp. 145 - 152 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Cambridge, UK
Cambridge University Press
14.07.2010
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Subjects | |
Online Access | Get full text |
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Abstract | Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty acid sensitivity, food selection and BMI in human subjects. The study included two parts; study 1 established in thirty-one subjects (29 (sem 1·4) years, 22·8 (sem 0·5) kg/m2) taste thresholds using 3-AFC (3-Alternate Forced Choice Methodology) for oleic, linoleic and lauric acids, and quantified oral lipase activity. During study 2, fifty-four subjects (20 (sem 0·3) years, 21·5 (sem 0·4) kg/m2) were screened for oral fatty acid sensitivity using oleic acid (1·4 mm), and they were defined as hypo- or hypersensitive via triplicate triangle tests. Habitual energy and macronutrient intakes were quantified from 2 d diet records, and BMI was calculated from height and weight. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat. Study 1 reported median lipase activity as 2 μmol fatty acids/min per l, and detection thresholds for oleic, linoleic and lauric acids were 2·2 (sem 0·1), 1·5 (sem 0·1) and 2·6 (sem 0·3) mm. Study 2 identified twelve hypersensitive subjects, and hypersensitivity was associated with lower energy and fat intakes, lower BMI (P < 0·05) and an increased ability to rank custards based on fat content (P < 0·05). Sensitivity to oleic acid was correlated to performance in the fat ranking task (r 0·4, P < 0·05). These data suggest that oral fatty acid hypersensitivity is associated with lower energy and fat intakes and BMI, and it may serve as a factor that influences fat consumption in human subjects. |
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AbstractList | Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty acid sensitivity, food selection and BMI in human subjects. The study included two parts; study 1 established in thirty-one subjects (29 (sem 1·4) years, 22·8 (sem 0·5) kg/m2) taste thresholds using 3-AFC (3-Alternate Forced Choice Methodology) for oleic, linoleic and lauric acids, and quantified oral lipase activity. During study 2, fifty-four subjects (20 (sem 0·3) years, 21·5 (sem 0·4) kg/m2) were screened for oral fatty acid sensitivity using oleic acid (1·4 mm), and they were defined as hypo- or hypersensitive via triplicate triangle tests. Habitual energy and macronutrient intakes were quantified from 2 d diet records, and BMI was calculated from height and weight. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat. Study 1 reported median lipase activity as 2 μmol fatty acids/min per l, and detection thresholds for oleic, linoleic and lauric acids were 2·2 (sem 0·1), 1·5 (sem 0·1) and 2·6 (sem 0·3) mm. Study 2 identified twelve hypersensitive subjects, and hypersensitivity was associated with lower energy and fat intakes, lower BMI (P < 0·05) and an increased ability to rank custards based on fat content (P < 0·05). Sensitivity to oleic acid was correlated to performance in the fat ranking task (r 0·4, P < 0·05). These data suggest that oral fatty acid hypersensitivity is associated with lower energy and fat intakes and BMI, and it may serve as a factor that influences fat consumption in human subjects. Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty acid sensitivity, food selection and BMI in human subjects. The study included two parts; study 1 established in thirty-one subjects (29 (sem 1.4) years, 22.8 (sem 0.5) kg/m2) taste thresholds using 3-AFC (3-Alternate Forced Choice Methodology) for oleic, linoleic and lauric acids, and quantified oral lipase activity. During study 2, fifty-four subjects (20 (sem 0.3) years, 21.5 (sem 0.4) kg/m2) were screened for oral fatty acid sensitivity using oleic acid (1.4 mm), and they were defined as hypo- or hypersensitive via triplicate triangle tests. Habitual energy and macronutrient intakes were quantified from 2 d diet records, and BMI was calculated from height and weight. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat. Study 1 reported median lipase activity as 2 mumol fatty acids/min per l, and detection thresholds for oleic, linoleic and lauric acids were 2.2 (sem 0.1), 1.5 (sem 0.1) and 2.6 (sem 0.3) mm. Study 2 identified twelve hypersensitive subjects, and hypersensitivity was associated with lower energy and fat intakes, lower BMI (P < 0.05) and an increased ability to rank custards based on fat content (P < 0.05). Sensitivity to oleic acid was correlated to performance in the fat ranking task (r 0.4, P < 0.05). These data suggest that oral fatty acid hypersensitivity is associated with lower energy and fat intakes and BMI, and it may serve as a factor that influences fat consumption in human subjects.Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty acid sensitivity, food selection and BMI in human subjects. The study included two parts; study 1 established in thirty-one subjects (29 (sem 1.4) years, 22.8 (sem 0.5) kg/m2) taste thresholds using 3-AFC (3-Alternate Forced Choice Methodology) for oleic, linoleic and lauric acids, and quantified oral lipase activity. During study 2, fifty-four subjects (20 (sem 0.3) years, 21.5 (sem 0.4) kg/m2) were screened for oral fatty acid sensitivity using oleic acid (1.4 mm), and they were defined as hypo- or hypersensitive via triplicate triangle tests. Habitual energy and macronutrient intakes were quantified from 2 d diet records, and BMI was calculated from height and weight. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat. Study 1 reported median lipase activity as 2 mumol fatty acids/min per l, and detection thresholds for oleic, linoleic and lauric acids were 2.2 (sem 0.1), 1.5 (sem 0.1) and 2.6 (sem 0.3) mm. Study 2 identified twelve hypersensitive subjects, and hypersensitivity was associated with lower energy and fat intakes, lower BMI (P < 0.05) and an increased ability to rank custards based on fat content (P < 0.05). Sensitivity to oleic acid was correlated to performance in the fat ranking task (r 0.4, P < 0.05). These data suggest that oral fatty acid hypersensitivity is associated with lower energy and fat intakes and BMI, and it may serve as a factor that influences fat consumption in human subjects. Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty acid sensitivity, food selection and BMI in human subjects. The study included two parts; study 1 established in thirty-one subjects (29 (sem 1.4) years, 22.8 (sem 0.5) kg/m2) taste thresholds using 3-AFC (3-Alternate Forced Choice Methodology) for oleic, linoleic and lauric acids, and quantified oral lipase activity. During study 2, fifty-four subjects (20 (sem 0.3) years, 21.5 (sem 0.4) kg/m2) were screened for oral fatty acid sensitivity using oleic acid (1.4 mm), and they were defined as hypo- or hypersensitive via triplicate triangle tests. Habitual energy and macronutrient intakes were quantified from 2 d diet records, and BMI was calculated from height and weight. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat. Study 1 reported median lipase activity as 2 mumol fatty acids/min per l, and detection thresholds for oleic, linoleic and lauric acids were 2.2 (sem 0.1), 1.5 (sem 0.1) and 2.6 (sem 0.3) mm. Study 2 identified twelve hypersensitive subjects, and hypersensitivity was associated with lower energy and fat intakes, lower BMI (P < 0.05) and an increased ability to rank custards based on fat content (P < 0.05). Sensitivity to oleic acid was correlated to performance in the fat ranking task (r 0.4, P < 0.05). These data suggest that oral fatty acid hypersensitivity is associated with lower energy and fat intakes and BMI, and it may serve as a factor that influences fat consumption in human subjects. Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty acid sensitivity, food selection and BMI in human subjects. The study included two parts; study 1 established in thirty-one subjects (29 ( sem 1·4) years, 22·8 ( sem 0·5) kg/m 2 ) taste thresholds using 3-AFC (3-Alternate Forced Choice Methodology) for oleic, linoleic and lauric acids, and quantified oral lipase activity. During study 2, fifty-four subjects (20 ( sem 0·3) years, 21·5 ( sem 0·4) kg/m 2 ) were screened for oral fatty acid sensitivity using oleic acid (1·4 m m ), and they were defined as hypo- or hypersensitive via triplicate triangle tests. Habitual energy and macronutrient intakes were quantified from 2 d diet records, and BMI was calculated from height and weight. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat. Study 1 reported median lipase activity as 2 μmol fatty acids/min per l, and detection thresholds for oleic, linoleic and lauric acids were 2·2 ( sem 0·1), 1·5 ( sem 0·1) and 2·6 ( sem 0·3) m m . Study 2 identified twelve hypersensitive subjects, and hypersensitivity was associated with lower energy and fat intakes, lower BMI ( P < 0·05) and an increased ability to rank custards based on fat content ( P < 0·05). Sensitivity to oleic acid was correlated to performance in the fat ranking task ( r 0·4, P < 0·05). These data suggest that oral fatty acid hypersensitivity is associated with lower energy and fat intakes and BMI, and it may serve as a factor that influences fat consumption in human subjects. Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty acid sensitivity, food selection and BMI in human subjects. The study included two parts; study 1 established in thirty-one subjects (29 (sem 1·4) years, 22·8 (sem 0·5) kg/m2) taste thresholds using 3-AFC (3-Alternate Forced Choice Methodology) for oleic, linoleic and lauric acids, and quantified oral lipase activity. During study 2, fifty-four subjects (20 (sem 0·3) years, 21·5 (sem 0·4) kg/m2) were screened for oral fatty acid sensitivity using oleic acid (1·4 mm), and they were defined as hypo- or hypersensitive via triplicate triangle tests. Habitual energy and macronutrient intakes were quantified from 2 d diet records, and BMI was calculated from height and weight. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat. Study 1 reported median lipase activity as 2 μmol fatty acids/min per l, and detection thresholds for oleic, linoleic and lauric acids were 2·2 (sem 0·1), 1·5 (sem 0·1) and 2·6 (sem 0·3) mm. Study 2 identified twelve hypersensitive subjects, and hypersensitivity was associated with lower energy and fat intakes, lower BMI (P < 0·05) and an increased ability to rank custards based on fat content (P < 0·05). Sensitivity to oleic acid was correlated to performance in the fat ranking task (r 0·4, P < 0·05). These data suggest that oral fatty acid hypersensitivity is associated with lower energy and fat intakes and BMI, and it may serve as a factor that influences fat consumption in human subjects. Fatty acids are the chemical moieties that are thought to stimulate oral nutrient sensors, which detect the fat content of foods. In animals, oral hypersensitivity to fatty acids is associated with decreased fat intake and body weight. The aims of the present study were to investigate oral fatty acid sensitivity, food selection and BMI in human subjects. The study included two parts; study 1 established in thirty-one subjects (29 (sem 1·4) years, 22·8 (sem 0·5) kg/m2) taste thresholds using 3-AFC (3-Alternate Forced Choice Methodology) for oleic, linoleic and lauric acids, and quantified oral lipase activity. During study 2, fifty-four subjects (20 (sem 0·3) years, 21·5 (sem 0·4) kg/m2) were screened for oral fatty acid sensitivity using oleic acid (1·4 mm), and they were defined as hypo- or hypersensitive via triplicate triangle tests. Habitual energy and macronutrient intakes were quantified from 2 d diet records, and BMI was calculated from height and weight. Subjects also completed a fat ranking task using custard containing varying amounts (0, 2, 6 and 10 %) of fat. Study 1 reported median lipase activity as 2 μmol fatty acids/min per l, and detection thresholds for oleic, linoleic and lauric acids were 2·2 (sem 0·1), 1·5 (sem 0·1) and 2·6 (sem 0·3) mm. Study 2 identified twelve hypersensitive subjects, and hypersensitivity was associated with lower energy and fat intakes, lower BMI (P < 0·05) and an increased ability to rank custards based on fat content (P < 0·05). Sensitivity to oleic acid was correlated to performance in the fat ranking task (r 0·4, P < 0·05). These data suggest that oral fatty acid hypersensitivity is associated with lower energy and fat intakes and BMI, and it may serve as a factor that influences fat consumption in human subjects. [PUBLICATION ABSTRACT] |
Author | Clifton, Peter M. Stewart, Jessica E. Keast, Russell S. J. Feinle-Bisset, Christine Golding, Matthew Delahunty, Conor |
Author_xml | – sequence: 1 givenname: Jessica E. surname: Stewart fullname: Stewart, Jessica E. organization: School of Exercise and Nutrition Sciences, Deakin University, Burwood, VIC 3125, Australia – sequence: 2 givenname: Christine surname: Feinle-Bisset fullname: Feinle-Bisset, Christine organization: Discipline of Medicine, Royal Adelaide Hospital, University of Adelaide, Adelaide, SA, Australia – sequence: 3 givenname: Matthew surname: Golding fullname: Golding, Matthew organization: Institute of Food, Nutrition and Human Health, Massey University, Palmerston North, New Zealand – sequence: 4 givenname: Conor surname: Delahunty fullname: Delahunty, Conor organization: CSIRO Food and Nutritional Sciences, Riverside Corporate Park, North Ryde, NSW, Australia – sequence: 5 givenname: Peter M. surname: Clifton fullname: Clifton, Peter M. organization: Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, University of Adelaide, Adelaide, SA, Australia – sequence: 6 givenname: Russell S. J. surname: Keast fullname: Keast, Russell S. J. email: russell.keast@deakin.edu.au organization: School of Exercise and Nutrition Sciences, Deakin University, Burwood, VIC 3125, Australia |
BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22963676$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/20196892$$D View this record in MEDLINE/PubMed |
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References | S0007114510000267_ref20 Imamurra (S0007114510000267_ref19) 1989; 35 (S0007114510000267_ref21) 1997 Beauchamp (S0007114510000267_ref15) 1990; 51 S0007114510000267_ref28 S0007114510000267_ref26 S0007114510000267_ref25 S0007114510000267_ref24 S0007114510000267_ref23 Bertino (S0007114510000267_ref27) 1982; 36 Mattes (S0007114510000267_ref29) 1993; 57 S0007114510000267_ref9 Gibson (S0007114510000267_ref32) 1993 S0007114510000267_ref31 S0007114510000267_ref4 S0007114510000267_ref30 S0007114510000267_ref3 S0007114510000267_ref2 (S0007114510000267_ref17) 1991 (S0007114510000267_ref22) 2006 S0007114510000267_ref1 Meilgaard (S0007114510000267_ref18) 2007 S0007114510000267_ref8 S0007114510000267_ref7 S0007114510000267_ref5 Fukuwatari (S0007114510000267_ref6) 1997; 414 S0007114510000267_ref16 S0007114510000267_ref14 S0007114510000267_ref13 S0007114510000267_ref12 S0007114510000267_ref11 S0007114510000267_ref33 S0007114510000267_ref10 |
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