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 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 mmol 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.
The dimeric ring-shaped sliding clamp of E. coli DNA polymerase III (beta subunit, homolog of eukaryotic PCNA) is loaded onto DNA by the clamp loader gamma complex (homolog of eukaryotic Replication Factor C, RFC). The delta subunit of the gamma complex binds to the beta ring and opens it. The crystal structure of a beta:delta complex shows that delta, which is structurally related to the delta' and gamma subunits of the gamma complex, is a molecular wrench that induces or traps a conformational change in beta such that one of its dimer interfaces is destabilized. Structural comparisons and molecular dynamics simulations suggest a spring-loaded mechanism in which the beta ring opens spontaneously once a dimer interface is perturbed by the delta wrench.
Objective: To evaluate the effects of a high-fat and low-fat diet on taste sensitivity to oleic acid (C18:1) in lean and overweight/ obese (OW/OB) subjects. Design: Randomized cross-over dietary intervention involving the consumption of a high-fat (445% fat) and low-fat (o20% fat) diet, both consumed over a 4-week period. Subjects: A total of 19 lean, mean age 33±13 years, mean body mass index (BMI) 23.2±2.2 kg m -2 and 12 OW/OB, mean age 39.5 ± 3 years, mean BMI 28 ± 2.6 kg m -2 , subjects participated in the study, which measured taste thresholds for C18:1, fat perception and hedonic ratings for regular (RF) and lowered-fat (LF) foods before, and following consumption of a high-and low-fat diet. Results: Consumption of the low-fat diet increased taste sensitivity to C18:1 among lean and OW/OB subjects (Po0.05) and increased the subjects ability to perceive small differences in the fat content of custard (P ¼ 0.05). Consumption of the high-fat diet significantly decreased taste sensitivity to C18:1 among lean subjects (Po0.05), with no change in sensitivity among OW/OB persons (P ¼ 0.609). The hedonic ratings for several RF and LF foods differed following the diets. Conclusion: Alterations in the fat content of the diet modulated taste sensitivity to C18:1 among lean subjects, which was increased following a 4-week period of fat restriction and attenuated following the high-fat diet. The failure of the high-fat diet to alter fatty acid taste thresholds among OW/OB subjects suggests that these individuals were 'adapted' to high-fat exposure, perhaps because of differences in habitual fat consumption. Taken together, these data suggest that excessive dietary fat attenuates nutrient sensing epithelia response in the oral cavity, which could be associated with changes in diet and weight status.
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