Abstract
Fatty acid (FA) chemoreception in the oral cavity, known as fat taste, may trigger a satiety response that is homologous to FA chemoreception in the gastrointestinal tract. In addition, individuals with an impaired fat taste sensitivity are more likely to have an impaired satiety response. This study aimed to assess the effect of an FA mouth rinse on self-reported appetite, and to determine if the effect is modified by fat taste sensitivity. Thirty-one participants (age, 32.0 ± 8.4 y; body mass index (BMI), 26.1 ± 8.1 kg/m2) were studied on four separate days to evaluate the effect of a 20 mM oleic acid (OA) mouth rinse (in duplicate) compared to a control (in duplicate) on self-reported appetite by using a visual analogue scale (VAS) every 30 min for three hours following a standardized low-fat breakfast. The area under the curve ratings for fullness were greater (p = 0.003), and those for hunger were lower (p = 0.002) following the OA rinse compared to the control. The effect of the OA rinse was greater in individuals who were hypersensitive to fat taste compared to moderately sensitive and hyposensitive individuals for fullness (p < 0.010) and hunger (p < 0.010) ratings. In summary, an OA mouth rinse decreases self-reported hunger and increases self-reported fullness, particularly in those who are more sensitive to fat taste. FA receptors in the oral cavity may be potential targets to regulate appetite.
Highlights
The chemoreception of fatty acid (FA) via FA receptors in the gastrointestinal tract (GIT) triggers satiety responses [1], triggering the release of satiety hormones [2,3] and the slowing of gastric emptying [4,5]
While most dietary fat is consumed in the form of triglyceride, triglycerides are hydrolyzed to FA by gastric lipases in the GIT [6] and, to a smaller degree, by salivary lipases in the oral cavity [7]
A recent study by our research group identified that homologous FA receptors on enteroendocrine cells in the GIT were housed within human taste papillae in the oral cavity [9], leading to the belief that the entire alimentary canal has a role in regulating food intake via nutrient sensing [10]
Summary
The chemoreception of fatty acid (FA) via FA receptors in the gastrointestinal tract (GIT) triggers satiety responses [1], triggering the release of satiety hormones [2,3] and the slowing of gastric emptying [4,5]. This signaling pathway exists to reduce subsequent appetite throughout and following an eating event [2]. A recent study by our research group identified that homologous FA receptors on enteroendocrine cells in the GIT were housed within human taste papillae in the oral cavity [9], leading to the belief that the entire alimentary canal has a role in regulating food intake via nutrient sensing [10].
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